Hi everyone,

I just thought I would update you all on what has happened to my
request for help through Disability payments. Well after the visit
from the Doctor I was not exactly ecstatic, BUT - surprise, surprise -
  I have actually been accepted.

That means I can get help for getting around (in England tht means
they will even help you with a chair or car) and because I only need
minimum help for my personal care I only got the lower rate of help.

It does take away some of the financial worry because it means that I
can apply for government help - which is limited, but better than I
thought.

So that news cheered me up a bit after what has been a few very
difficult weeks in my life. I am still having difficulties in coming
to terms with the fact that I will probably never be able to work
again, but it has removed a lot of the stress in life. Just got to
sort out the finances now!

I hope all is well, I find everyone quite quiet in here for the
moment! Welcome to all the newbies and gentle hugs to everyone!

Cynthia

Dear Louise,

I'm not in the UK, but like Cynthia (Feisty) I do take Tramadol.  It
doesn't completely eradicate the pain, but makes it more manageable.
Anti-inflammatories (only one I can take so far is Diclofenac) help too.

Judi in Indiana US
(where it is gone back to hot and humid again!)

Hi Dorrit,

You are absolutely right. It is antibiotics which can give you
candida. Indeed, I think - or thought - that is where it all started.
I had a really bad throat and the antibiotics the doctor gave me
first I had a bad reaction to, then I had a second lot, then a third
different lot again. Then the candidosis kicked in  and boy - I will
never forget it. They even had to pierce my eardrums (paracentesis)
to let our the fungal infection!

So I had massive doses of antifungal medecine, then intestinal flora
type medication then they put me on longterm antibiotics for what
they perceived to be systemic infection following all that. (I ate
tons of natural yogurt every day to avoid reinfecting with candida.)
I guess I will never know really what happened and I am trying to
piece together the different incidents in my life that might have
some meaning today.

The long and the short of it is that I will never really know - I am
just guessing at possibilities.

I have done some more reading today an I still think there might be
something in this.

Just my opinion though......

Cynthia

  --- In Dercums_Disease@yahoogroups.com, "Dorrit Hvam" <fiori68@y...>
wrote:
> Hi Cynthia,
> i must admit you lost me along the way, very long ago. I am not
into
> all these things. Just wondered that your candida was treated with
> antibiotics. From my experience it is the other way round - you are
> treated with antibiotics for some reason and get candida as a side
> effect.....
>
> I still remember at the back of my head (very much back) reading
> about mycoplasma and longtermed treatment with penicillin. Am I the
> only survivor here from say 5 yrs back???
> Where did the others go? Cured or dead or just giving up??
>
> Dorrit - trying to think
>
>
> --- In Dercums_Disease@yahoogroups.com, "feisty_in_yorks"
> <c_prentice2003@y...> wrote:
> > Hi Dorrit,
> >
> > The testing is hugely difficult and has to be done in very
> specialised
> > laboratories and although everybody carries these microbacteria,
> it
> > seems that they take advantage when the immune system is running
> low -
> > forany reason.
> >
> > The treatment of these mycoplasmas takes at least 12 months of
the
> > Tetracycline antibobiotic group, and often goes on for 18 months.
> > Sometimes they become immune to one type and the treatment has to
> be
> > changed to another similar group (the name of which escapes me at
> the
> > untimely hour on Sunday morning!).
> >
> > I know that I have never been tested but I did have to take
> antibiotics
> > for what doctors thought was systemic infection after having a
> total
> > body infection of candida (eyes, ears, nose, throat, intestines,
> > everywhere) and I can remember thinking that 3 months of
> antibiotics
> > would wreak havoc in my body - but it did not and I definitely
> felt
> > better after the treatment. However, as I said, a few months
later
> I
> > started to get eye infections (not candida based) followed by
> severe
> > chest infections (Something I have never been prone to).
> >
> > Doctors just said that my body had been weakened by antibiotics
> for too
> > long and that these were oportunistic infections. It makes sense
> to me
> > today, that all of these were due to an invisible agent - such as
> these
> > mycoplasmas - because as I was in Corsica, there were no
> specialised
> > labs to do this kind of testing. Over a period of three to four
> years I
> > got better but have never had the constitution I had before all
> that.
> >
> > I have not seen any posts on this on here before, but I have only
> been
> > here since December last year and the names you mention do not
> mean
> > anything to me. I would love to know what any outcomes were
though.
> >
> > When you read through all the "odd illnesses" that seem to infect
> us
> > all - on top of the DD - then I just wonder whether there are a
> form of
> > mycoplasma at the root. Perhaps not the direct cause but a
> contributing
> > factor, the way they are in cancer and in heart disease. Perhaps
> we
> > are "lucky" enough to have immune systems which stop them from
> acting
> > the way they do in cancer (imitating the DNA behaviour in
> reproducing
> > the cells as malignant and then multiplying) and this is causing
> > the "healthy" fat cells to become larger than normal and forming
> more
> > easily into lipomas or angiolipomas. Perhaps this is the body's
> natural
> > way of quarantining the changed cells into groups together and
> > therefore forming lipomas to avoid the cells being carried around
> to
> > metastise the way the do in cancer. Just my mind wandering and
> using a
> > lot of imagination......
> >
> > I am still reading and trying to digest what I can on the medical
> > stuff - but it still would seem to be a contributing factor
which -
>
> > linked to hereditary prediposition and perhaps a hereditary lack
> of
> > immunity to these mycoplasmas would cause some people to fight
> them off
> > and others to be affected across a whole family. After all the is
> a
> > hereditary factor in cancer, which can apparently be triggered by
> these
> > mycoplasmas. And the Helicopter Pylori mycoplasma is the reason
> for
> > very many heart complaints....... This was only discovered
> relatively
> > recently.
> >
> > Do any of you know any family friends who are Doctors??
> >
> > Cynthia
> >
> > --- In Dercums_Disease@yahoogroups.com, "Dorrit Hvam"
> <fiori68@y...>
> > wrote:
> > > Maybe I am totally wrong, but something tells me that the
> subject of
> > > mycoplasma has been brought up before. Was it in connection
with
> the
> > > projects of Dr. Martin and Jamie Sams? He talked about stealth
> virus,
> > > but who mentioned mycoplasma?
> > > Dr. Martin's clinic was closed due to lack of recognition I
> think,
> > and
> > > we never heard from Jamie Sams anymore.
> > >
> > > Sorry, my brains have moved elsewhere tonight.
> > >
> > > But I believe I was tested for mycoplasma about 6 yrs ago in
> > > connection with a hospital stay. Negative.
> > >
> > > Does anyone of the veterans remember anything about this?
> > >
> > > Brainless Dorrit

Hi Luoise,

I have tried and tested all the over the counter analgesics only to
find little relief. I have been prescribed higher doses over codeine
mix tablets but support them very badly.

Now I am on Tramadol - slow-release and I have found this to be much
better - although the pain exceeds its capacity to calm sometimes. I
have persmission to take extra if needed but have tried not to!

I forgot twice and will never forget again - believe me!

Cynthia

--- In Dercums_Disease@yahoogroups.com, "manzilou" <loumanzi@t...>
wrote:
> Hi, can i just ask the people in the UK what medication they find
helps
> the pain of DD please from Louise.

Hi Cynthia,
i must admit you lost me along the way, very long ago. I am not into
all these things. Just wondered that your candida was treated with
antibiotics. From my experience it is the other way round - you are
treated with antibiotics for some reason and get candida as a side
effect.....

I still remember at the back of my head (very much back) reading
about mycoplasma and longtermed treatment with penicillin. Am I the
only survivor here from say 5 yrs back???
Where did the others go? Cured or dead or just giving up??

Dorrit - trying to think


--- In Dercums_Disease@yahoogroups.com, "feisty_in_yorks"
<c_prentice2003@y...> wrote:
> Hi Dorrit,
>
> The testing is hugely difficult and has to be done in very
specialised
> laboratories and although everybody carries these microbacteria,
it
> seems that they take advantage when the immune system is running
low -
> forany reason.
>
> The treatment of these mycoplasmas takes at least 12 months of the
> Tetracycline antibobiotic group, and often goes on for 18 months.
> Sometimes they become immune to one type and the treatment has to
be
> changed to another similar group (the name of which escapes me at
the
> untimely hour on Sunday morning!).
>
> I know that I have never been tested but I did have to take
antibiotics
> for what doctors thought was systemic infection after having a
total
> body infection of candida (eyes, ears, nose, throat, intestines,
> everywhere) and I can remember thinking that 3 months of
antibiotics
> would wreak havoc in my body - but it did not and I definitely
felt
> better after the treatment. However, as I said, a few months later
I
> started to get eye infections (not candida based) followed by
severe
> chest infections (Something I have never been prone to).
>
> Doctors just said that my body had been weakened by antibiotics
for too
> long and that these were oportunistic infections. It makes sense
to me
> today, that all of these were due to an invisible agent - such as
these
> mycoplasmas - because as I was in Corsica, there were no
specialised
> labs to do this kind of testing. Over a period of three to four
years I
> got better but have never had the constitution I had before all
that.
>
> I have not seen any posts on this on here before, but I have only
been
> here since December last year and the names you mention do not
mean
> anything to me. I would love to know what any outcomes were though.
>
> When you read through all the "odd illnesses" that seem to infect
us
> all - on top of the DD - then I just wonder whether there are a
form of
> mycoplasma at the root. Perhaps not the direct cause but a
contributing
> factor, the way they are in cancer and in heart disease. Perhaps
we
> are "lucky" enough to have immune systems which stop them from
acting
> the way they do in cancer (imitating the DNA behaviour in
reproducing
> the cells as malignant and then multiplying) and this is causing
> the "healthy" fat cells to become larger than normal and forming
more
> easily into lipomas or angiolipomas. Perhaps this is the body's
natural
> way of quarantining the changed cells into groups together and
> therefore forming lipomas to avoid the cells being carried around
to
> metastise the way the do in cancer. Just my mind wandering and
using a
> lot of imagination......
>
> I am still reading and trying to digest what I can on the medical
> stuff - but it still would seem to be a contributing factor which -

> linked to hereditary prediposition and perhaps a hereditary lack
of
> immunity to these mycoplasmas would cause some people to fight
them off
> and others to be affected across a whole family. After all the is
a
> hereditary factor in cancer, which can apparently be triggered by
these
> mycoplasmas. And the Helicopter Pylori mycoplasma is the reason
for
> very many heart complaints....... This was only discovered
relatively
> recently.
>
> Do any of you know any family friends who are Doctors??
>
> Cynthia
>
> --- In Dercums_Disease@yahoogroups.com, "Dorrit Hvam"
<fiori68@y...>
> wrote:
> > Maybe I am totally wrong, but something tells me that the
subject of
> > mycoplasma has been brought up before. Was it in connection with
the
> > projects of Dr. Martin and Jamie Sams? He talked about stealth
virus,
> > but who mentioned mycoplasma?
> > Dr. Martin's clinic was closed due to lack of recognition I
think,
> and
> > we never heard from Jamie Sams anymore.
> >
> > Sorry, my brains have moved elsewhere tonight.
> >
> > But I believe I was tested for mycoplasma about 6 yrs ago in
> > connection with a hospital stay. Negative.
> >
> > Does anyone of the veterans remember anything about this?
> >
> > Brainless Dorrit

Hi, can i just ask the people in the UK what medication they find helps
the pain of DD please from Louise.

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Hello , here is a interesting article on EBV< please
read because it does mention  something about a human
tumour virus. Mine has become alot worse that is why I
have not been on .. also I read EBV can trigger MS.
  test results  .
6/28/05                      7/22/05
EBV  IgG  ANTIBODIES          EBV  IgG       nOMAL
1:640                           1:2560        < 1:10
TITER

EBV  EARLY ANTIGEN IgG
1:40                             1:160          <1:10

EBV NUCLEAR ANTIGEN IgG           1:80           <1:5
  1:80


   STILL VERY ACTIVE, FEEL LIKE CRAP , ORGANS FEEL LIKE
THEY ARE GOING TO EXPLODE .. ANYWAY pcp WANTS ME TO
SEE RHEUMATOLOGIST, WHICH IS 8/4 NO ONE HAS SEEN ME
SINCE i GOT THIS AND MY ANA ARES HIGH ALSO .. WELL
TALK TO YOU ALL SOON..



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From: "Barb croker" <lyonziefiddler@...>  Add
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To: wcroker@..., lyonziefiddler@...
Subject: EBV
Date: Thu, 28 Jul 2005 15:42:48 -0400


eMedicine World Medical Library

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	 Home  |  Specialties | Resource Centers |  CME  |
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	 July 28, 2005
   Articles Images CME Advanced Search  Consumer Health
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site
Back to: eMedicine Specialties > Pediatrics >
Infectious Diseases

Mononucleosis and Epstein-Barr Virus Infection
Last Updated: October 5, 2004
Rate this Article
Email to a Colleague
Synonyms and related keywords: EBV, acute infectious
mononucleosis,
infectious mononucleosis, mono, human herpesvirus 4,
HHV-4, kissing
disease

  	 AUTHOR INFORMATION  Section 1 of 10    Click here
to go to the next
section in this topic
Author Information Introduction Clinical Differentials
Workup Treatment
Medication Follow-up Miscellaneous Bibliography

Author: Glenna B Winnie, MD, Director, Division of
Pulmonology,
Associate
Professor, Department of Pediatrics, University of
Pittsburgh and
Children's
Hospital of Pittsburgh

Glenna B Winnie, MD, is a member of the following
medical societies:
American Academy of Pediatrics, American College of
Physician
Executives,
American Lung Association, American Society for
Microbiology, American
Thoracic Society, and Society for Pediatric Research

Editor(s): Rosemary Johann-Liang, MD, Medical Officer,
Infectious
Diseases
and Pediatrics, Division of Special Pathogens and
Immunological Drug
Products, Center for Drug Evaluation and Research,
Food and Drug
Administration; Mary L Windle, PharmD, Adjunct
Assistant Professor,
University of Nebraska Medical Center College of
Pharmacy, Pharmacy
Editor,
eMedicine.com, Inc; Mark R Schleiss, MD, American
Legion Chair of
Pediatrics, Professor of Pediatrics, Division
Director, Division of
Infectious Diseases and Immunology, Department of
Pediatrics,
University of
Minnesota School of Medicine; Robert W Tolan, Jr, MD,
Chief of Allergy,
Immunology, and Infectious Diseases, The Children's
Hospital at St
Peter's
University Hospital, Clinical Associate Professor of
Pediatrics, Drexel
University College of Medicine; and Russell Steele,
MD, Professor and
Vice
Chairman, Department of Pediatrics, Head, Division of
Infectious
Diseases,
Louisiana State University Health Sciences Center



Disclosure
  	 INTRODUCTION  Section 2 of 10   Click here to go to
the previous
section
in this topic Click here to go to the top of this page
Click here to go
to
the next section in this topic
Author Information Introduction Clinical Differentials
Workup Treatment
Medication Follow-up Miscellaneous Bibliography

Background: Epstein-Barr virus (EBV), or human
herpesvirus 4, is a
gamma-herpesvirus that infects more than 95% of the
world's population.
The
most common manifestation of primary infection with
this organism is
acute
infectious mononucleosis, a self-limited clinical
syndrome that most
frequently affects adolescents and young adults.
Classic symptoms
include
sore throat, fever, and lymphadenopathy. Infection
with EBV in younger
children usually is asymptomatic or mild. However, EBV
also is a human
tumor
virus, the first virus associated with human
malignancy. Infection with
EBV
is associated with lymphoproliferative disorders,
especially in
immunocompromised hosts, and with a variety of tumors
including
nasopharyngeal carcinoma and Burkitt lymphoma.

Acute infectious mononucleosis first was described in
the late 19th
century
as acute glandular fever, an illness consisting of
lymphadenopathy,
fever,
hepatosplenomegaly, malaise, and abdominal discomfort
in adolescents
and
young adults. In 1920, Sprunt and associates applied
the name
infectious
mononucleosis to cases of spontaneously resolving
acute leukemia
associated
with blastlike cells in the blood. Downey described
the lymphocyte
morphology in 1923. In 1932, Paul and Bunnell
discovered that serum
from
symptomatic patients had antibodies that agglutinate
the red blood
cells
(RBCs) of unrelated species, the heterophile
antibodies. This allowed
enhanced diagnostic accuracy of infectious
mononucleosis.

The search for the etiologic agent of infectious
mononucleosis was
unsuccessful for many years, partly because
researchers did not
appreciate
that most primary infections are asymptomatic and that
most adults are
seropositive. In 1964, Epstein described the first
human tumor virus
when he
found virus particles in a Burkitt lymphoma cell line.
Henle reported
the
relationship between acute infectious mononucleosis
and EBV in 1968.
Subsequently, a large prospective study of students at
Yale University
firmly established EBV as the etiologic agent of
infectious
mononucleosis.

Pathophysiology: Humans are the only known reservoir
of EBV. EBV is
present
in oropharyngeal secretions and most commonly is
transmitted through
saliva.
After initial inoculation, the virus replicates in
nasopharyngeal
epithelial
cells. Cell lysis is associated with release of
virions, with viral
spread
to contiguous structures, including salivary glands
and oropharyngeal
lymphoid tissues. Further viral replication results in
viremia, with
subsequent infection of the lymphoreticular system,
including the
liver,
spleen, and B lymphocytes in peripheral blood. Host
immune response to
the
viral infection includes CD8-positive T lymphocytes
with suppressor and
cytotoxic functions, the characteristic atypical
lymphocytes found in
the
peripheral blood. The T lymphocytes are cytotoxic to
the EBV-infected B
cells and eventually reduce the number of EBV-infected
B lymphocytes to
less
than 1 per 106 circulating B cells.

Primary infection with EBV is followed by latent
infection, a
characteristic
of herpesviruses. After acute EBV infection, latently
infected
lymphocytes
and epithelial cells persist and are immortalized. In
vivo, this allows
perpetuation of infection, while in vitro,
immortalized cell lines are
established. During latent infection, the virus is
present in the
lymphocytes and oropharyngeal epithelial cells as
episomes in the
nucleus.
These episomes rarely integrate into the cell genome
but do replicate
with
cell division and are passed to subsequent generations
of cells. A low
rate
of viral reactivation occurs within the population of
latently infected
cells. Epithelial cells are the primary source of new
virus in latently
infected individuals, infecting B cells as they
circulate through the
oropharynx.

Two strains labeled EBV-1 and EBV-2 (also known as
type A and type B)
exist.
Although some differences are present in the genes
expressed during
latent
infection, no apparent differences exist in acute
illnesses caused by
the 2
strains. Both strains are prevalent throughout the
world and can
simultaneously infect the same person.

Knowledge of the structure of EBV and which proteins
are expressed
during
different stages of its life cycle is required to
understand the
laboratory
tests used to determine if an individual has primary
acute,
convalescent,
latent, or reactivation infection. A mature infectious
viral particle,
which
may be present in the cytoplasm of an epithelial cell,
consists of a
nucleoid, a capsid, and an envelope. The nucleoid
contains linear
double-stranded viral deoxyribonucleic acid (DNA). It
is surrounded by
the
capsid, an icosahedral constructed of capsomers, which
are tubular
protein
subunits. An envelope derived either from the outer
membrane or the
nuclear
membrane of the host cell encloses the capsid and
nucleoid, ie, the
nucleocapsid. The envelope also contains viral
proteins that were
constructed and placed in the host cell membrane
before viral assembly
began.

To initiate cellular infection, a viral particle
attaches via its major
outer envelope glycoprotein, ie, gp350/220, to the EBV
receptor CD21 on
a B
lymphocyte. The binding site on epithelial cells is
not certain but
also may
be CD21. EBV then is internalized into cytoplasmic
vesicles. After
fusion of
virus envelope with the vesicle membrane, the
nucleocapsid is released
into
the cytoplasm. The nucleocapsid dissolves, the genome
is transported to
the
cell nucleus, and the linear genome then circularizes,
forming an
episome.
The cell then may proceed with either lytic infection
with release of
infectious virus or latent infection of the host cell.
B lymphocytes
with
latent infection undergo growth transformation.

Lytic infection occurs early after primary
inoculation. As a result of
lytic
infection in oral epithelial cells, EBV can be found
in the saliva for
the
first 12-18 months after acquisition. Thereafter,
epithelial cells and
lymphocytes are latently infected, with a few
spontaneously converting,
leading to viral replication, host cell lysis and
death, and release of
mature virions. Thus, virus can be isolated from oral
secretions of
20-30%
of healthy latently infected individuals at any time.

During latent infection, cell proteins are expressed
in 1 of 3
patterns.
Type I latency, associated with Burkitt lymphoma, is
characterized by
expression of only EBV-encoded ribonucleic acids
(RNAs), Epstein-Barr
early
regions (EBERs), and Epstein-Barr nuclear antigen 1
(EBNA1). Type II
latency, associated with nasopharyngeal carcinoma, is
characterized by
expression of 3 latent membrane proteins, LMP1, LMP2A,
and LMP2B, plus
EBERs
and EBNA1. Type III latency is the pattern found in
healthy individuals
with
latent infection. In addition to the EBERs and EBNA1
expressed in type
I
latency, other nuclear antigens (including EBNA2,
EBNA3A, EBNA3B,
EBNA3C,
and LMP) are expressed in type III latency.

Frequency:

     * In the US: EBV is not a reportable infection,
and exact frequency
of
symptomatic primary infection is not known. By age 5
years,
approximately
50% of the US population is infected. During
childhood, primary
infection
usually is asymptomatic or associated with mild
elevation of liver
function
tests. EBV infection acquired during adolescence is
asymptomatic or
associated with the syndrome of acute infectious
mononucleosis.

       Incidence of acute infectious mononucleosis was
approximately 45
cases
per 100,000 population per year in the early 1970s,
with the highest
incidence in individuals aged 15-24 years. However,
changes in economic
status may have changed both the age of initial
infection and the
incidence
of infectious mononucleosis since the large
epidemiologic studies were
completed. In lower socioeconomic groups, EBV
infection is more common,
occurs at an earlier age, and is less likely to be
associated with
acute
infectious mononucleosis.

       Roommates of students with primary EBV infection
develop
seroconversion at the same rate as the general
population of college
students.

       Approximately 90% of the US population is
infected with EBV by
age 25
years.

       EBV infection does not occur in epidemics, and
it is of
relatively low
transmissibility.

     * Internationally: EBV infection occurs with the
same frequency and
symptomatology in the developed nations of the world
as in the United
States.

       EBV more frequently is acquired in childhood in
underdeveloped
nations, and therefore the syndrome of acute
infectious mononucleosis
is
unusual in these nations.

       In Africa, the virus is associated with endemic
Burkitt lymphoma.

       High numbers of EBV episomes are found in the
cells of
undifferentiated or poorly differentiated
nasopharyngeal carcinoma.
This is
the most common tumor in adult men in southern China,
and it also
occurs
frequently in North American Inuits and North African
whites.

Mortality/Morbidity:

     * Most primary EBV infections are asymptomatic.
Death is unusual in
the
immunocompetent patient with acute infectious
mononucleosis, but it may
occur due to neurologic complications, upper airway
obstruction, or
splenic
rupture.

     * EBV infection is linked with a number of tumors.
Endemic Burkitt
lymphoma, the most common tumor of childhood in
Africa, is associated
with
EBV and malaria. Infection with Plasmodium falciparum
malaria
stimulates
polyclonal B cell proliferation with EBV infection and
impairs T
lymphocyte
response to EBV, apparently contributing to tumor
pathogenesis. In
Asia, EBV
infection is related to development of nasopharyngeal
carcinoma. Most
non-Hodgkin lymphomas are associated with EBV, and
evidence of the EBV
genome is demonstrable in many of these tumors. EBV
also is associated
with
Hodgkin lymphoma, where EBV genome is present in the
Reed-Sternberg
cell.

     * EBV infection in patients who are
immunocompromised is associated
with
several syndromes and proliferative disorders.

           o Individuals with Duncan syndrome, ie,
X-linked
lymphoproliferative syndrome, may develop fatal
primary EBV infection
due to
a defect in immune response to EBV. These boys often
develop fatal
massive
hepatitis or a disseminated lymphoproliferative
disorder triggered by
primary EBV infection. Median age of presentation is
2.5 years, with
median
survival of 33 days. Survivors of the initial
infection develop B-cell
lymphoma or hypogammaglobulinemia and usually die by
age 10 years.

           o Other congenital immunodeficiencies are
associated with the
development of EBV-associated lymphoproliferative
disorders. These
include
ataxia-telangiectasia, Chédiak-Higashi syndrome,
Wiskott-Aldrich
syndrome,
and common variable immunodeficiency.

           o Posttransplant lymphoproliferative
disorder (PTLD) is a
potentially fatal lymphoproliferative syndrome
associated with EBV and
monoclonal or polyclonal expansion of B cells. It
occurs in patients
after
organ transplantation, particularly after heart
transplants, and
usually
responds to decreased immune suppression.

           o EBV-associated lymphomas occur in patients
with secondary
immunodeficiencies (eg, after cancer chemotherapy).
Unfortunately,
these
tumors do not respond to lessening of
immunosuppression.

           o In patients with AIDS, EBV is associated
with hairy
leukoplakia,
leiomyosarcoma, CNS lymphoma, and with lymphoid
interstitial
pneumonitis in
children.

Race:

     * No racial predilection exists.

     * Large epidemiologic studies performed in the
1970s revealed that
acute
infectious mononucleosis was 30 times more likely to
occur in whites
than in
African Americans. However, this correlated with lower
social economic
status and earlier asymptomatic infection in African
Americans and
therefore
did not reflect a true racial difference.

Sex:

     * No sexual predilection exists.

     * Incidence of infectious mononucleosis is the
same in men and
women,
although the peak incidence occurs 2 years earlier in
females.

Age:

     * EBV infection usually occurs during infancy or
childhood and
remains
latent through life.

     * In developed nations, infection may not occur
until adolescence
or
adulthood, and approximately 50% of adolescents who
acquire EBV develop
the
infectious mononucleosis syndrome.

     * Acute infectious mononucleosis has been reported
in middle-aged
and
elderly adults, and usually they are heterophile
antibody negative.



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History:

     * Acute infectious mononucleosis presents with a
history of 1-2
weeks of
fatigue and malaise; however, onset may be abrupt.

     * Incubation period in adolescents is 30-50 days;
it is shorter in
young
children.

     * Symptoms include sore throat, headache, fever,
myalgias, nausea,
and
abdominal pain.

     * Sore throat is the most frequent presenting
symptom. Gradually
worsening over the first week, it may be the most
severe sore throat
the
patient has experienced.

     * Headache usually occurs during the first week
and may be
retro-orbital.

     * Left upper quadrant pain may be due to splenic
enlargement.
Abdominal
pain should lead to consideration of splenic rupture.

     * Symptoms usually persist for 2-3 weeks, but
fatigue often is more
prolonged.

     * Infants and young children with primary
infection usually are
asymptomatic.

Physical:

     * Infectious mononucleosis is characterized by
pharyngitis,
generalized
lymphadenopathy, and hepatosplenomegaly. Most clinical
symptoms are a
consequence of T cell proliferation and organ
infiltration.

     * Pharyngitis is the most consistent physical
finding.

           o Pharyngitis is exudative in one third of
patients.

           o Petechiae are present at the junction of
the hard and soft
palates in 25-60% of patients.

           o Tonsillar enlargement can be massive, and
occasionally it
causes
airway obstruction. The enlargement can be associated
with dehydration
due
to difficulty in swallowing.

     * Lymphadenopathy is prominent, and most commonly
it affects the
posterior cervical lymph nodes. Anterior cervical and
submandibular
nodal
involvement is common, and axillary and inguinal nodes
also are
affected.

           o Enlarged epitrochlear nodes are very
suggestive of
infectious
mononucleosis.

           o Nodal enlargement usually is symmetric.

           o Nodes are mildly tender to palpation and
are freely
moveable.

     * Hepatomegaly frequently is present, but jaundice
is rare.
Percussion
tenderness over the liver is common.

     * Splenomegaly is common. The spleen often is
palpable 2-3 cm below
the
left costal margin and may be tender.

           o The spleen enlarges rapidly over the first
week of
symptoms,
usually decreasing in size over the next 7-10 days.

           o The spleen can rupture from relatively
minor trauma or even
spontaneously.

     * Fever occurs in more than 90% of patients.
Temperature peaks in
the
afternoon, typically at 38-39°C, but it may reach
40°C. Fever resolves
over
10-14 days.

     * Despite fever, pulse usually is normal or
relatively low, and
pulse
rate over 100 is unusual.

     * Maculopapular rash (usually faint, widely
scattered, and
erythematous)
occurs in 3-15% of patients and is more common in
young children.

           o Treatment with amoxicillin or ampicillin
is associated with
rash
in approximately 80% of patients.

           o Circulating immunoglobulin G (IgG) and
immunoglobulin M
(IgM)
antibodies to ampicillin are demonstrable.

     * Eyelid edema may be present, especially in the
first week of
illness.

     * Children younger than 4 years more commonly have
splenomegaly or
hepatomegaly, rash, and symptoms of an upper
respiratory tract
infection.

Causes:

     * EBV is the etiologic agent in approximately 90%
of acute
infectious
mononucleosis cases.

     * Cytomegalovirus (CMV) is most commonly
associated with
EBV-negative
infectious mononucleosis syndrome.

     * Other viruses associated with a similar acute
illness include
adenovirus; hepatitis A, hepatitis B, or hepatitis C;
herpes simplex 1
and
herpes simplex 2; human herpesvirus 6; rubella; and
primary human
immunodeficiency virus in adolescents or young adults.

     * Etiology of most EBV-negative infectious
mononucleosis cases
remains
unknown.



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Hepatitis A
Hepatitis B
Hepatitis C
Herpes Simplex Virus Infection
Herpesvirus 6 Infection
Human Immunodeficiency Virus Infection
Streptococcal Infection, Group A
Toxoplasmosis


Other Problems to be Considered:

Drug reaction to phenytoin of sulfa
Lymphoma
Acute Myelocytic Leukemia
Acute Lymphoblastic Leukemia
Adenovirus
Rubella


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Hepatitis A

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  	 WORKUP  Section 5 of 10   Click here to go to the
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Lab Studies:

     * Classic criteria: The 3 classic criteria for
laboratory
confirmation
of acute infectious mononucleosis are (1)
lymphocytosis, (2) the
presence of
at least 10% atypical lymphocytes on peripheral smear,
and (3) a
positive
serologic test for EBV.

     * Complete blood count

           o Leukocytosis with white blood cell (WBC)
count of
10,000-20,000
cells per cm3 (10-20 X 109/L) occurs in 40-70% of
patients with acute
infectious mononucleosis. By the second week of
illness, approximately
10%
have a WBC count greater than 25,000 per cm3.

           o Approximately 80-90% of patients have
lymphocytosis, with
greater than 50% lymphocytes. Lymphocytosis is
greatest during the
second
and third weeks of illness and lasts for 2-6 weeks.
Usually 20-40% of
the
lymphocytes are atypical, although not all patients
have more than 10%
atypical lymphocytes.

             The atypical lymphocytes of 3 Downey types
are larger, have
a
lower nuclear-to-cytoplasmic ratio, and have a less
dense nucleus than
normal lymphocytes. Most of these atypical lymphocytes
are
polyclonal-activated CD8 cytotoxic-suppressor T
lymphocytes, although
CD4
helper T cells and CD11 natural killer cells also are
present.

           o Mild thrombocytopenia occurs in 25-50% of
patients.

     * Liver function tests

           o Most (ie, 80-100%) patients with acute
infectious
mononucleosis
have elevated liver function test results.

           o Alkaline phosphatase, aspartate
aminotransferase (AST), and
bilirubin peak 5-14 days after onset, and
gamma-glutamyltransferase
(GGT)
peaks at 1-3 weeks.

           o Lactic (acid) dehydrogenase (LDH) is
increased in
approximately
95% of patients.

           o Occasionally, GGT remains mildly elevated
for up to 12
months,
but most liver function test results are normal by 3
months.

     * Heterophile antibody test

           o EBV infection stimulates polyclonal
secretion of antibodies
by
infected B cells, including transient production of
heterophile
antibodies.
These are antibodies that agglutinate cells from other
species and are
not
directed against EBV. The Paul-Bunnell test for
heterophile antibodies
is
based on the fact that serum from patients with acute
mononucleosis
contains
antibodies that agglutinate sheep RBCs in a tube
dilution assay, while
such
antibodies are absent from or present in a low titer
in serum from
healthy
persons.

           o Differential absorption

                 + Antibodies other than those produced
during acute
infectious mononucleosis can agglutinate sheep RBCs.
Such antibodies
include
those formed in serum sickness, during drug reactions,
and naturally
occurring antibodies to the Forssman antigen.

                 + Differential absorption permits
identification of the
antibody type. Bovine RBCs absorb infectious
mononucleosis heterophile
antibodies from serum, but not Forssman antibodies.
Guinea pig kidney
cells
absorb Forssman antibodies, leaving the infectious
mononucleosis
heterophile
antibodies. Antibodies formed in serum sickness absorb
to both guinea
pig
kidney cells and to bovine RBCs. Thus, in terms of
absorbing infectious
mononucleosis heterophile antibodies, clinicians use
the saying, "cow
can,
pig can't."

                 + Serum from a patient with infectious
mononucleosis
agglutinates sheep RBCs after absorption with guinea
pig cells, but no
agglutination occurs after absorption with bovine
RBCs.

           o Heterophile antibody titers

                 + The titer of
Paul-Bunnell—heterophile antibody is
determined by tube dilution. Depending on the dilution
system, a titer
of
1:40 or 1:28 after absorption with guinea pig cells is
considered
positive
for acute infectious mononucleosis.

                 + Titer level does not correlate with
severity of
clinical
illness.

           o Monospot

                 + Rapid slide agglutination tests,
including Monospot
assays, have been developed to measure acute
infectious mononucleosis
heterophile antibodies in a rapid qualitative fashion.
Slide tests use
either horse RBCs or bovine RBCs. Horse RBCs are more
sensitive than
sheep
RBCs or bovine RBCs and can be treated with formalin
to extend the
shelf
life of the test. Bovine RBCs are specific for acute
infectious
mononucleosis heterophile antibodies and thus do not
require
differential
absorption.

                 + All commercial kits for rapid
diagnosis of acute
infectious mononucleosis heterophile antibodies have
low sensitivity
(63-84%), with a negative predictive value of more
than 10%.

                 + Spot tests have rare false-positive
results in
patients
with lymphoma or hepatitis.

           o Frequency of positive heterophile
antibodies

                 + Heterophile antibodies are
measurable in
approximately 50%
of patients in the first week of illness, and 60-90%
of patients have
positive test results for heterophile antibodies in
the second or third
weeks. The titer begins to decline during the fourth
or fifth week and
often
is less than 1:40 by 2-3 months after symptom onset.

                 + As many as 20% of patients have
positive titers 1-2
years
after acquisition. Also, because horse RBC agglutinins
are more
sensitive
than sheep RBCs, 75% of patients have positive horse
RBC agglutinins at
1
year.

                 + Only 10-30% of children younger than
2 years and
50-75% of
children aged 2-4 years develop heterophile antibodies
with primary EBV
infection.

     * EBV serology

           o Infection with EBV is characterized by
development of the
specific antibodies to antigenic components of the
virus. These
antigens
appear at different stages of infection and differ in
lytic versus
latent
infection.

           o Antibodies to EBV antigens measured for
clinical purposes
are
those to viral capsid antigen (VCA), early antigens
(EAs), and
Epstein-Barr
nuclear antigen (EBNA).

                 + EAs are expressed early in the lytic
cycle, while VCA
and
membrane antigens are structural viral proteins
expressed late in the
lytic
cycle.

                 + EBNA is expressed in cells that are
latently
infected.

                 + Antibodies to membrane antigens
usually are not
measured,
but their presence correlates with viral neutralizing
activity.

                 + Antibodies to these proteins are
measured by enzyme
immunoassays, indirect immunofluorescence assays, and
immunoblot
assays.

           o With early infection, EAs are expressed in
cells in the
lytic
cycle. These antigens are nonstructural EBV proteins,
which are
classified
into 2 groups based on cell distribution and stability
with methanol
treatment.

                 + The restricted component of early
antigens (EA/R) is
found
in the cytoplasm of infected cells and is methanol
sensitive. Antibody
to
EA/R most often is measurable in children younger than
4 years with
primary
EBV infection or in nonsymptomatic infection.

                 + Approximately 80% of patients with
infectious
mononucleosis have antibodies to the diffuse-staining
component of EA
(EA/D).

                 + EA/D antibodies are elevated in
patients with
nasopharyngeal carcinoma, and antibodies to EA/R are
high in
individuals
with EBV-associated Burkitt lymphoma. Patients who are

immunocompromised and
have persistent or reactivated EBV infections often
have high antibody
levels to EA/D or EA/R.

           o Time course of antibody production

                 + In early primary EBV infection,
oropharyngeal
epithelial
cells are lytically infected, and the above antigens
are expressed.
Antibodies are measurable at the onset of clinical
symptoms or even
slightly
before.

                 + Although not always measurable,
antibody to EA is
rising
at symptom onset. EA/D is observed more frequently,
although EA/R is
present
more often in asymptomatic infection or in children
younger than 4
years.
Levels of antibody to EA rise for 3-4 weeks, then
usually quickly
decline to
undetectable levels by 3-4 months, although low levels
may be detected
intermittently for years. However, in patients with a
more prolonged
symptomatic illness, EA/D may become unmeasurable, and
EA/R may become
positive.

                 + VCA-IgM usually is measurable at
symptom onset, peaks
at
2-3 weeks, then declines and becomes unmeasurable by
3-4 months.
VCA-IgG
rises shortly after symptom onset, peaks at 2-3
months, then drops
slightly
but persists for life. Antibodies to EBNA appear
during convalescence
and
remain present for life.

     * Interpretation of EBV serology: Primary acute
EBV infection is
associated with VCA-IgM, VCA-IgG, and absent EBNA
antibodies.

           o Antibody pattern in recent infection (3-12
mo) includes
positive
VCA-IgG and EBNA antibodies, negative VCA-IgM
antibodies, and usually
positive EA antibodies.

           o After 12 months, the pattern is the same
as recent
infection,
except EA antibodies are not present.

Imaging Studies:

     * No specific imaging studies are indicated for
making the
diagnosis of
acute infectious mononucleosis.

     * Chest radiograph (CXR) shows mediastinal
adenopathy in fewer than
1%
of patients. Mediastinal lymph node enlargement should
prompt
consideration
of other diagnoses.

     * Abdominal CT scan is the preferred imaging
modality to assess for
splenic rupture but can be performed only in patients
who are
hemodynamically stable. Ultrasonography or
radionuclide scanning of the
spleen also may assist in ascertaining the diagnosis.

     * Lateral neck films are occasionally helpful to
document tonsillar
hypertrophy and exclude epiglottis in a patient with
upper airway
obstruction or stridor.

     * Imaging studies for PTLD: In PTLD, CXR may
reveal nodular
lesions.
Chest CT scan with contrast may show the
characteristic peripheral
nodules,
and abdominal CT scan with contrast can define the
extent of
intra-abdominal
lesions.

Other Tests:

     * Quantitative polymerase chain reaction (PCR) can
measure EBV DNA
in
plasma during acute infectious mononucleosis. Levels
decline during
convalescence and are not measurable in latently
infected individuals.
However, EBV DNA in serum may be detectable by PCR
with reactivation of
infection, such as in PTLD.

     * Epstein-Barr early region (EBER) probe can
identify the EBV
messenger
RNA in the nuclei of EBV-infected lymphoid cells by in
situ
hybridization.

Histologic Findings: EBV infection is characterized by
the presence of
atypical lymphocytes in the peripheral blood. The
cells are activated
CD8 T
cells, which are not infected, but rather are
mobilized to destroy the
infected B cells.

During acute mononucleosis, lymph nodes are increased
in size, with
enlarged
germinal centers and lymphoid follicles.
Perifollicular areas of the
tonsils
contain many infected B lymphocytes, which express
EBV-specific
antigens,
including LMP1, EBNA1, and EBNA2.

The spleen is larger with lymphocytic infiltration of
the capsule and
trabeculae. Pleomorphic blast cells are present in the
hyperplastic red
pulp. Vascular congestion is coupled with focal and
subcapsular
hemorrhages.

Histologic changes in the liver usually are minimal
with mild swelling
in
hepatic sites and bile ducts and lymphocytic portal
infiltration.

In fatal infectious mononucleosis, degenerative
changes are observed in
the
neurons of the CNS. Neuronal degeneration,
perivascular cuffing, and
astrocytic hyperplasia may be present.

PTLD is characterized by homogeneous lymphocytic
proliferation with an
immunoblastic component. Lesions may efface lymphoid
organ architecture
or
develop ectopically in nonlymphoid organs. The
EBV-infected cells in
PTLD
express EBER.

  	 TREATMENT  Section 6 of 10   Click here to go to
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Medical Care:

     * Infectious mononucleosis is a self-limited
illness that usually
does
not require specific therapy.

     * Because of low transmissibility of EBV,
isolation is not
indicated.

     * Most affected individuals can be evaluated and
treated as
outpatients.
Inpatient therapy of medical and surgical
complications may be
required.

Surgical Care:

     * Splenic rupture is an acute abdominal emergency
that usually
requires
surgical intervention.

           o Rupture may occur with trauma as minor as
palpation, and
sometimes it is the presenting complaint.

           o Diagnosis can be confirmed by imaging
procedures or by
peritoneal lavage in an unstable patient.

           o Splenectomy usually is required.

           o Occasionally, observation and supportive
measures are
adequate
treatment for a hemodynamically stable patient.

           o Although partial splenectomy or suturing
the capsular tear
has
been advocated to preserve splenic function, the acute
changes that led
to
rupture militate against the success of this approach.

Consultations:

     * Surgical consultation should be sought when the
patient has
abdominal
pain or evidence of shock.

     * Consultation with the appropriate subspecialist
is indicated for
management of significant complications.

Diet:

     * No dietary modifications are required.

Activity:

     * Acceptable activity level during the acute
illness depends on
severity
of the patient's symptoms.

     * Extreme fatigue may require bed rest for 1-2
weeks.

     * Malaise may persist for 2-3 months, and activity
can increase as
tolerated.

     * Patients should not participate in contact
sports or heavy
lifting for
at least 2-3 weeks, although some authors recommend
avoiding activities
that
may cause splenic trauma for 2 months.



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  	 MEDICATION  Section 7 of 10   Click here to go to
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Acute infectious mononucleosis is treated
symptomatically. NSAIDs are
used
to treat fever and discomfort. Corticosteroids do not
significantly
alter
the course of infectious mononucleosis. Although they
ameliorate
symptoms,
do not use corticosteroids in the treatment of
uncomplicated disease.
They
are used in the presence of significant upper airway
obstruction due to
tonsillar or lymph node hypertrophy and in severe
thrombocytopenia or
hemolytic anemia.
A number of drugs inhibit EBV replication in vitro.
Nonetheless,
antiviral
agents are of no benefit in uncomplicated infectious
mononucleosis.
However,
antiviral agents are used in the treatment of
interstitial pneumonitis,
X-linked lymphoproliferative syndrome, PTLD, and other

lymphoproliferative
disorders. Intravenous immunoglobulin may be
considered to modulate
immune
function in the presence of disease complications due
to
autoantibodies.
New therapies, including the use of interferon alpha
and the infusion
of
donor T cells or EBV-specific cytotoxic T cells, are
being studied.

Drug Category: Glucocorticoids -- Corticosteroids are
potent
anti-inflammatory drugs that also modify the immune
response. They are
used
to decrease the size of tonsils and upper airway lymph
nodes in the
presence
of airway compromise and possible upper airway
obstruction. They may be
useful to treat severe thrombocytopenia or hemolytic
anemia. Whether
prednisone should be used for myocarditis,
pericarditis, or CNS system
involvement is unclear.
Drug Name
	 Prednisone (Deltasone, Liquid Prep, Meticorten,
Orasone, Prednicen-M,
Sterapred) -- May decrease inflammation by reversing
increased
capillary
permeability and suppressing PMN activity.
Adult Dose 60-80 mg/d PO divided bid for 5-7 d; taper
over 1-2 wk
Pediatric Dose 1 mg/kg/d PO divided bid, not to exceed
60-80 mg;
administer
for 5-7 d, then taper over 1-2 wk
Contraindications Systemic fungal infections;
varicella; vaccination
with
live or live-attenuated vaccines
Interactions Immune response to vaccinations may be
impaired;
phenytoin,
rifampin, or drugs that induce hepatic enzymes can
decrease serum
concentration
Pregnancy C - Safety for use during pregnancy has not
been established.
Precautions Associated with multiple adverse
reactions, including fluid
and
electrolyte disturbances and musculoskeletal
abnormalities including
muscle
weakness, steroid myopathy, and osteoporosis; GI
adverse effects
include
peptic ulcer disease, pancreatitis, and an increase in
LFTs; steroid
use has
been associated with increased intracranial pressure,
seizures,
headache,
growth suppression, adrenal cortical suppression,
menstrual
irregularities,
hyperglycemia, negative nitrogen balance, glaucoma,
and cataracts
Drug Category: Antiviral drugs -- A number of drugs
inhibit EBV
replication
in vitro. These include acyclovir, desciclovir,
ganciclovir,
interferon-alfa, interferon-gamma, adenine
arabinoside, and
phosphonoacetic
acid. Placebo-controlled clinical trials have been
conducted for
infectious
mononucleosis only with acyclovir, which inhibits
viral shedding from
the
oropharynx. However, clinical course is not affected
significantly in
uncomplicated infectious mononucleosis.
Drug Name
	 Acyclovir (Zovirax) -- Strains of HSV1 are most
sensitive, followed by
HSV2. Also sensitive to other herpesviruses,
including, in descending
order,
varicella zoster, EBV, and CMV.
Adult Dose 800 mg PO 5 times/d for 10 d
10 mg/kg/dose IV q8h for 7-10 d
Pediatric Dose >24 months: 800 mg PO 5 times/d for 10
d, not to exceed
80
mg/kg/d in 5 divided doses; 10 mg/kg/dose IV q8h for
7-10 d
Contraindications Documented hypersensitivity
Interactions Neurotoxicity can occur when combined
with zidovudine;
probenecid decreases renal clearance of acyclovir; use
with
cyclosporine
increases risk of nephrotoxicity
Pregnancy B - Usually safe but benefits must outweigh
the risks.
Precautions Caution with other nephrotoxic drugs or in
those with
preexisting renal disease; maintain adequate urine
output for the first
2 h
after IV infusion; use carefully in patients with
renal, hepatic, or
electrolyte disturbances and in patients with
hypoxemia or underlying
neurologic abnormalities
Drug Category: Immunoglobulins -- Intravenous
immunoglobulin is used to
modulate immune function in the presence of
autoantibodies. It has been
used
successfully in the treatment of immune
thrombocytopenia associated
with
infectious mononucleosis.
Drug Name
	 Intravenous immunoglobulin (Gamimune N, Gammagard
S/D, Gammar-P,
Polygam)
-- Neutralizes circulating myelin antibodies through
antiidiotypic
antibodies; down-regulates proinflammatory cytokines,
including
INF-gamma;
blocks Fc receptors on macrophages; suppresses inducer
T and B cells
and
augments suppressor T cells; blocks complement
cascade; promotes
remyelination; may increase CSF IgG (10%).
Adult Dose 400 mg/kg/d IV for 2-5 d
Pediatric Dose Administer as in adults
Contraindications Documented hypersensitivity; IgA
deficiency
Interactions May interfere with antibody response to
live virus
vaccines
Pregnancy C - Safety for use during pregnancy has not
been established.
Precautions Hypersensitivity reactions may occur;
initiating at rate of
administration may increase risk of hypotension; risk
of anaphylaxis is
greater in IgA-deficient individuals (procure
low-titer IgA product if
essential)


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Further Inpatient Care:

     * Patients with uncomplicated infectious
mononucleosis rarely
require
inpatient therapy.

     * Hospitalization is warranted in the presence of
splenic rupture,
airway compromise, dehydration, significant
thrombocytopenia or
hemolytic
anemia, and neurologic or other major complications.

Further Outpatient Care:

     * If diagnosis is firmly established, only
supportive care is
required
in the absence of significant complications.

In/Out Patient Meds:

     * Nonspecific treatment includes saline gargles
and acetaminophen
or
ibuprofen for sore throat, fever, and myalgia.
Constipation may be
treated
with a laxative.

     * Corticosteroids decrease the duration of febrile
illness and
constitutional symptoms, but their routine use for
treatment of a virus
known to be related to tumor development is
discouraged.

     * Acyclovir has no demonstrable benefit for
treatment of
uncomplicated
infectious mononucleosis in placebo-controlled trials.

     * Various therapies are used for complications of
EBV infection,
although only a few have been studied in controlled
trials.

           o Corticosteroids are used for treatment of
severe airway
obstruction due to tonsillar enlargement, hemolytic
anemia, and severe
thrombocytopenia.

           o Interferon-alfa decreases shedding of EBV
in renal
transplant
recipients.

           o Acyclovir and desciclovir can reverse
EBV-associated hairy
leukoplakia in patients with HIV. Acyclovir has been
used for treatment
of
interstitial pneumonitis, X-linked lymphoproliferative
syndrome, and
lymphoproliferative disorders. PTLD has been treated
with ganciclovir
and
CytoGam.

           o Immune thrombocytopenia has been treated
with intravenous
immunoglobulin.

           o Whether corticosteroids are beneficial or
harmful in
encephalitis, pericarditis, and myocarditis is
unclear.

           o Combination therapy with corticosteroids
and acyclovir has
been
reported, with varying outcomes.

Transfer:

     * Transfer to a tertiary care center may be
necessary for treatment
of
significant complications.

Deterrence/Prevention:

     * Isolation is not required. EBV is of low
transmissibility and
cannot
be recovered from environmental surfaces or fomites.

     * Avoid contact with saliva.

           o EBV is present in throat washings of
individuals with acute
infectious mononucleosis. Virus can be cultured from
the oropharynx for
up
to 18 months. It can be recovered from the oropharynx
of 10-20% of
healthy
adults.

           o EBV infection usually is acquired through
contact between a
susceptible individual and the saliva of an
asymptomatic individual who
is
shedding EBV. In young children, saliva is spread by
drooling and
hand-to-mouth behaviors. In adolescents, infected
saliva may be
transferred
by kissing, hence the label "kissing disease."

     * Do not kiss children on the mouth.

     * Maintain clean conditions, especially when young
children are
present
(eg, in day care), and avoid having children share
toys.

     * EBV can be transmitted by blood transfusion and
by bone marrow
transplantation. However, because the organism is so
common, presently
no
procedures are in place to prevent this.

     * Vaccine development is proceeding, although the
role of a vaccine
is
unclear.

Complications:

     * Hepatitis occurs in more than 90% of patients
with infectious
mononucleosis.

           o Liver function test results are mildly
elevated but usually
are
no more than 2-3 times normal. Bilirubin is elevated
in approximately
45% of
patients, but jaundice occurs in only 5%.

           o Liver abnormalities are most pronounced in
the second and
third
weeks of illness.

     * Mild thrombocytopenia occurs in approximately
50% of patients
with
infectious mononucleosis.

           o Platelet count usually is
100,000-140,000/cm3. Platelet
count
usually reaches its nadir approximately 1 week after
symptom onset,
then
gradually improves over the next 3-4 weeks.

           o Thrombocytopenia may be caused by the
production of
antiplatelet
antibodies and peripheral destruction, especially in
the enlarged
spleen.

     * Hemolytic anemia occurs in 0.5-3% of patients
with infectious
mononucleosis.

           o Hemolytic anemia has been associated with
cold-reactive
antibodies, anti-I antibodies, and with autoantibodies
to triphosphate
isomerase.

           o Hemolysis usually is mild and is most
significant during
the
second and third weeks of symptoms.

     * Upper airway obstruction due to hypertrophy of
tonsils and other
lymph
nodes of Waldeyer ring occurs in 0.1-1% of patients.

           o Treatment with corticosteroids may be
beneficial.

           o Patients with severe tonsillar and lymph
node enlargement
with
impending airway obstruction may require intubation or
tracheostomy.

           o Patients requiring hospitalization may
have concurrent
streptococcal pharyngitis. Two thirds of patients
admitted with
infectious
mononucleosis with upper airway obstruction and
dehydration have
alpha-hemolytic Streptococcus infection, usually due
to group C
streptococci.

     * Splenic rupture occurs in 0.1-0.2% of patients
with infectious
mononucleosis.

           o Rupture may be spontaneous, although often
the patient has
a
history of some antecedent trauma.

           o Rupture is most likely to occur during the
second and third
weeks of clinical symptoms.

           o Patients can present with mild-to-severe
abdominal pain
below
the left costal margin, sometimes with radiation to
the left shoulder
and
supraclavicular area. Massive bleeding may be
accompanied by peritoneal
irritation and shifting dullness. Shock may be the
only presenting
symptom.

           o Because bradycardia is usual in infectious
mononucleosis,
tachycardia with pulse higher than 100 is an important
sign.

           o Neutrophilia, instead of lymphocytosis,
can occur.

           o Surgical intervention usually is required.

     * Hematologic complications are as follows:

           o EBV has been implicated in hemophagocytic
syndrome.

           o Immune thrombocytopenic purpura occurs and
may evolve to
aplastic anemia. Aplastic anemia and neutropenia
sometimes are
associated
with antineutrophil antibodies.

           o EBV infection may accelerate hemolytic
anemia in congenital
spherocytosis or hereditary elliptocytosis.

           o Disseminated intravascular coagulation
associated with
hepatic
necrosis has occurred.

     * Neurologic complications are as follows:

           o Neurologic complications occur in less
than 1% of EBV
infections
and usually develop during the first 2 weeks of EBV
infection. In some
patients, especially children, the neurologic symptoms
are the only
clinical
manifestation of infectious mononucleosis. Patients
often are negative
for
the heterophile antibody. However, these complications
often are
severe.
Complete recovery is the rule, but fatalities do
occur.

           o Primary EBV infection has been associated
with aseptic
meningitis, acute viral encephalitis, coma,
meningitis, and
meningoencephalopathy. Hypoglossal nerve palsy, Bell
palsy, hearing
loss,
brachial plexus neuropathy, and multiple cranial nerve
palsies have
been
described. Guillain-Barré syndrome, autonomic
neuropathy,
gastrointestinal
dysfunction secondary to selective cholinergic
dysautonomia, acute
cerebellar ataxia, and transverse myelitis have been
reported.
Metamorphopsia, ie, Alice in Wonderland syndrome, has
been described.

     * Cardiac and pulmonary complications are as
follows:

           o Pulmonary complications are extremely
rare, although upper
airway obstruction due to lymphoid hypertrophy is
relatively common.
Chronic
interstitial pneumonitis and pleural effusion have
been associated with
EBV
infection.

           o Cardiac abnormalities that can occur with
EBV infection
include
myocarditis and pericarditis.

     * Autoimmune complications are as follows:

           o Autoimmune diseases and Reye syndrome have
been associated
with
EBV infection.

           o Infectious mononucleosis stimulates
production of many
antibodies not directed against EBV. These include
autoantibodies,
anti-I
antibodies, cold hemolysins, antinuclear antibodies,
rheumatoid
factors,
cryoglobulins, and circulating immune complexes. These
antibodies may
precipitate autoimmune syndromes.

     * Miscellaneous complications are as follows:

           o Renal disorders associated with EBV
infection include
immune
deposit nephritis, renal failure, and paroxysmal
nocturnal
hemoglobinuria.

           o After cardiac bypass or transfusion, an
infectious
mononucleosis–like syndrome has been described. EBV
may cause this, but
it
more commonly is associated with primary
cytomegalovirus CMV infection.

           o A syndrome of chronic fatigue, myalgias,
sore throat, and
mild
cognitive dysfunction occurring primarily in young
adult females
initially
was attributed to EBV. Current data suggest that EBV
is not the
etiologic
agent.

Prognosis:

     * Immunocompetent individuals with acute
infectious mononucleosis
have a
good prognosis with full recovery expected within
several months.

     * The common hematologic and hepatic complications
resolve in 2-3
months.

     * Neurologic complications usually resolve quickly
in children.
Adults
are more likely to be left with neurologic deficits.

     * All individuals develop latent infection, which
usually remains
asymptomatic.

Patient Education:

     * Educate patient and family about risk of splenic
rupture and the
need
to refrain from contact sports for 2 months.

     * Inform patient and family about usual course of
symptoms with
acute
mononucleosis.

     * For excellent patient education resources, visit
eMedicine's
Bacterial
and Viral Infections Center. Also, see eMedicine's
patient education
article
Mononucleosis.

  	 MISCELLANEOUS  Section 9 of 10   Click here to go
to the previous
section
in this topic Click here to go to the top of this page
Click here to go
to
the next section in this topic
Author Information Introduction Clinical Differentials
Workup Treatment
Medication Follow-up Miscellaneous Bibliography

Medical/Legal Pitfalls:

     * Failure to recognize splenic rupture

     * Failure to recognize impending airway
obstruction

  	 BIBLIOGRAPHY  Section 10 of 10   Click here to go
to the previous
section
in this topic Click here to go to the top of this page
Author Information Introduction Clinical Differentials
Workup Treatment
Medication Follow-up Miscellaneous Bibliography

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15;
259(3): 384-8[Medline].
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the EBNA 3 family of nuclear proteins. J Virol 1989
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174(2):
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NOTE:
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therapies are
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therapies daily.
The
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and is generally
accepted within medical standards at the time of
publication. However,
as
medical science is constantly changing and human error
is always
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the authors, editors, and publisher or any other party
involved with
the
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Hi all -- I just joined. I was reading thru posts here raising
questions about weird kinds of things like mycoplasmas, and I
recalled
something I had read recently that mentioned mycoplasmas raining from
the skies, and the topic is chemtrails. It is very possible the skies
all over the planet are being sprayed with weird organisms and this
could be a reason why we are getting sick with weird conditions. One
site name is "Chemtrails 911 - Intro to Chemtrails". There are
actually
a lot of sites reporting on this possible phenomenon. Just google for
chemtrails. I didn't like reading  about it, but at the same time, if
it is true, it could explain a bit of what is going on. Antidote for
all the exposure to weird organisms is to build up the immune system
as
much as possible. I read about that too. Seems like colloidal silver
is
being tooted as a major immune booster. Also flax seed oil for
omega-3
fatty acid, also vit C, etc.

Hi everyone,

You are probably thinking I have nothing else to do but all of this
new searching started when my Rheum. said he did not need to see me
anymore because he does not think I have Systemic Lupus and that DD
is not his problem (sic)!

Well he did explain that he retested my bloods for Lupus (auto-
antibody for double-stranded DNA) because it had come back positive
last time. Only slightly positive - but he had been worried because
he had made me stop the medication I have been on for 5 years. He
cross-checked it and the other one was negative so he concluded that
the first one was a false positive. Well my husband said jokingly to
me "What if he is wrong and the second one was a false negative?"

That got me thinking and I found myself delving through reams of
medical papers on the subject of both. WELL !! I have just found out
that false posivity for Lupus comes up often on the Elisa tests
because it is highly sensitive and picks up an antibody to Rheumatoid
Arthritis and shows it as positive (when remember they are looking
for Lupus).

Which brings me back to what I have thought for months now......
perhaps I have Ankylosing Spondilitis like Dora, like so many others
who come in here........ Excrutiating back pain and wrists are not
even touched by the Tramadol (well just a little - as I found out
when I forgot to take it). He keeps insisting that this is only
Fibromyalgia.......

Well tomorrow I have an MRI scan for that tumour in my buttock but as
it covers across my hips, I will be asking them for any signs of AS.
Then he will be seeing me whether he likes it or not!!!!

Anybody else had negative ANAs but positive Anti-DNAs ?

Still searching (nothing else to do but freeze in 60 degree weather
in England !) High summer ......... yeahhhhhhhh

Cynthia

Hi Dorrit,

The testing is hugely difficult and has to be done in very specialised
laboratories and although everybody carries these microbacteria, it
seems that they take advantage when the immune system is running low -
forany reason.

The treatment of these mycoplasmas takes at least 12 months of the
Tetracycline antibobiotic group, and often goes on for 18 months.
Sometimes they become immune to one type and the treatment has to be
changed to another similar group (the name of which escapes me at the
untimely hour on Sunday morning!).

I know that I have never been tested but I did have to take antibiotics
for what doctors thought was systemic infection after having a total
body infection of candida (eyes, ears, nose, throat, intestines,
everywhere) and I can remember thinking that 3 months of antibiotics
would wreak havoc in my body - but it did not and I definitely felt
better after the treatment. However, as I said, a few months later I
started to get eye infections (not candida based) followed by severe
chest infections (Something I have never been prone to).

Doctors just said that my body had been weakened by antibiotics for too
long and that these were oportunistic infections. It makes sense to me
today, that all of these were due to an invisible agent - such as these
mycoplasmas - because as I was in Corsica, there were no specialised
labs to do this kind of testing. Over a period of three to four years I
got better but have never had the constitution I had before all that.

I have not seen any posts on this on here before, but I have only been
here since December last year and the names you mention do not mean
anything to me. I would love to know what any outcomes were though.

When you read through all the "odd illnesses" that seem to infect us
all - on top of the DD - then I just wonder whether there are a form of
mycoplasma at the root. Perhaps not the direct cause but a contributing
factor, the way they are in cancer and in heart disease. Perhaps we
are "lucky" enough to have immune systems which stop them from acting
the way they do in cancer (imitating the DNA behaviour in reproducing
the cells as malignant and then multiplying) and this is causing
the "healthy" fat cells to become larger than normal and forming more
easily into lipomas or angiolipomas. Perhaps this is the body's natural
way of quarantining the changed cells into groups together and
therefore forming lipomas to avoid the cells being carried around to
metastise the way the do in cancer. Just my mind wandering and using a
lot of imagination......

I am still reading and trying to digest what I can on the medical
stuff - but it still would seem to be a contributing factor which -
linked to hereditary prediposition and perhaps a hereditary lack of
immunity to these mycoplasmas would cause some people to fight them off
and others to be affected across a whole family. After all the is a
hereditary factor in cancer, which can apparently be triggered by these
mycoplasmas. And the Helicopter Pylori mycoplasma is the reason for
very many heart complaints....... This was only discovered relatively
recently.

Do any of you know any family friends who are Doctors??

Cynthia

--- In Dercums_Disease@yahoogroups.com, "Dorrit Hvam" <fiori68@y...>
wrote:
> Maybe I am totally wrong, but something tells me that the subject of
> mycoplasma has been brought up before. Was it in connection with the
> projects of Dr. Martin and Jamie Sams? He talked about stealth virus,
> but who mentioned mycoplasma?
> Dr. Martin's clinic was closed due to lack of recognition I think,
and
> we never heard from Jamie Sams anymore.
>
> Sorry, my brains have moved elsewhere tonight.
>
> But I believe I was tested for mycoplasma about 6 yrs ago in
> connection with a hospital stay. Negative.
>
> Does anyone of the veterans remember anything about this?
>
> Brainless Dorrit

Hi -- I just joined this group, thx to Cyn in Yorkshire letting me
about about it. I have one lipoma on my thigh, which has grown
steadily
since last November. The costochrondritis statement caught my
attention -- a surgeon recently told me my chest pains(one side)
might
be called that. I was also diagnosed with fibromyalgia a long time
ago.
However, here is my theory on what that is: I think it could be
candidiasis, which is an overgrowth of yeast in the intestines. This
condition is indicated by a craving for everything the yeast wants,
which is sugar and yeast and fermented foods. I went on the
noncandida-
feeding diet(no bread, sugar, fermented foods) and four months later,
the pain all over my body went down by 50% Then I lost the diet. It's
a
hard one to stay on. The theory goes that the yeast puts out at least
300 toxins into the body's tissues, and also undigested food gets out
of the intestines into the body's tissues, which then put up an
immune
response to it. If you study any book about candida, you'll see that
all systems of the body can be affected by this condition. That's why
we can have so many different kinds of symptoms and problems. This so
far is the global theory connecting the various disease syndromes for
me. -- Robin in San Francisco

--- In Dercums_Disease@yahoogroups.com, "nonny46" <nonny46@y...>
wrote:
> Dear group,
>
> I came across this in doing some research on "connective tissue:"
>
> http://www.medisurf.co.kr/Category/category.asp?GENE_NO=D002015&gp=1
>
> where it mentions that DD is "auto-immune" and other interesting
> facts.  I got started on the search because of being told my chest
> pains experienced recently were probably costochondritis, which is
an
> inflammation of connective tissue.
>
> Now I have started thinking that since fibromyalgia is considered
> a "connective tissue disorder" and apparently so is DD!  Not simply
the
> lumps and aches and pains, but the connective tissue as well.  I'm
sure
> soomeone has probably brought this up before, but I never had the
> similarities of the two diseases hit me right in the face like
this.
> Too bad that the treatments for fibro don't necessarily help DD.
>
> Judi (with too much time on my hands)

Maybe I am totally wrong, but something tells me that the subject of
mycoplasma has been brought up before. Was it in connection with the
projects of Dr. Martin and Jamie Sams? He talked about stealth virus,
but who mentioned mycoplasma?
Dr. Martin's clinic was closed due to lack of recognition I think, and
we never heard from Jamie Sams anymore.

Sorry, my brains have moved elsewhere tonight.

But I believe I was tested for mycoplasma about 6 yrs ago in
connection with a hospital stay. Negative.

Does anyone of the veterans remember anything about this?

Brainless Dorrit

These words sort of wrote themselves last night, so I thought I'd share
them with you.  It's for those times when we feel like we're not the
person we'd like to be.

In my mind...

I can dance, jump, whirl.
I can run, hike, ride a horse or a bike.
I can carry a sleeping child upstairs.
I can build a house,
I can walk briskly, untiring.
I can skydive, parasail, river raft.
I can climb mountains, up and down.

Maybe only in my mind, but that's enough...for now.

Judi

Hi Catherine,

I have seen dozens (If not hundreds) of different Doctors, having
lived in France where there is open access to Consultants. All this
has done was repeat dozens of times different blood tests (sometimes
with wildly varying results!) and NEVER to come to a conclusion. I
was diagnosed 5 years ago with Lupus, but it seems that even that is
a misdiagnosis.

I would definitely ask to se a Dermatologist at your nearest Teaching
hospital. Insist to your GP and don't let it drop. It can take months
to get an appointment so insist upon the urgency for the pain. I have
been referred for over two years now but am only just into the
sausage machine - if you know what I mean! Having said that - in the
last two weeks I have been told by both the Derm. and the Rheum. that
they can do no more for me.....


Surgery seems to be the only option here in GB - and only if they
deem the pain to be bad enough.Where is the nearest Teaching Hosp. to
you - Lancaster?

Keep in touch - we have to stick together...

Cynthia

--- In Dercums_Disease@yahoogroups.com, "Catherene Smith"
<atbi68@d...> wrote:
>  HI Cynthia,
>
> Thank you for the welcome to the group, and for the info links.
>
> I live in Morecambe, and see your email addy is York's is that as in
> Yorkshire or in York.
>
> I would like to know how you got diagnosed with Dercums , I am
wondering if
> I should ask to be referred to  Rheumatology , would that be the
right
> people to diagnose this.
>
>
>  Hi Renee,
>
> Welcome to our group. I am in the UK too, so go ahead and ask any
> questions. I will answer what I can.
>
> I, too, have had this disease for over 25 years but have only had a
> diagnosis for 6 months.

Dear Renee,

Welcome to the group from another Smith!  I live in the US (southern
Indiana, about 50 miles from anything) but my Dad's grandfather came
from Scotland.  I was born a Smith and married a Smith :o)

One does not necessarily HAVE to be overweight to have Dercum's--there
are a number of people in this group who are not overweight.  I wasn't
awfully heavy when I first started manifesting the more painful
symptoms of the disease, but am now about 30 lb. overweight (due mostly
to inactivity and just plain stress eating.)  I have started the South
Beach (low G.I.) diet and have lost nearly 20 lb.

As Cynthia suggested, there are good resources here for you, and
hopefully you will find a doctor who can diagnose you.  You are
definitely NOT an idiot!  Good luck,

Judi

Hi Renee,

Welcome to our group. I am in the UK too, so go ahead and ask any
questions. I will answer what I can.

I, too, have had this disease for over 25 years but have only had a
diagnosis for 6 months. I have been treated like an idiot too many
times to remember and I can honestly say that I was near to meltdown
when I found this group!.

You must go to these sites and print out as much info. as possible.
Share it with your sister because you will soon see that it is nigh-
on impossible to find decent info on the net, if you do not know
where to look.

www.dercumshope.org

www.lipomaforum.com

On these sites you will find all sorts of info and help. We chat on
Thursday evenings at 19h00 British Summer Time so log in and ask the
questions....

You will soon see how fantastic these people are - we are all in the
same boat - and it is reassuring to see you are no longer alone.

I did all this, then went to the Doctor and said, "I am not mad, I am
not depressed - Please do not insult my intelligence by saying these
lumps are in my head and are not painful. Here are some  documents on
Dercum's Disease, please take a look and tell me what you think."

That's what I did - with the help of all these wonderful people. So I
finally got a firm diagnosis - but as you will soon see - we have no
research (or very little), so no cure..... Just pain control. But
that is better than disbelief and insults and makes things slightly
better. The possibility of excision (surgery) is good if they get
everything or if the lipoma is on a nerve - but there seems to be a
substantial possibility of return of the lipomas, so it has to be
weighed up.

Take care and please join in our discussions - (they really are a
lovely bunch in here )!

Cynthia

--- In Dercums_Disease@yahoogroups.com, "Renee smith" <atbi68@d...>
wrote:
> Hello everyone,
>
> My name is Renee, and I have joined your group in hope I can find
> help in UK.
>
> I have been ill for a great number of years, and been classed as an
> idiot by most doctors I have seen.
>
> I was diagnosed with Fybromyalga, a long time ago,and recently my
> sister was told she had Dercums Disease and she is convinced this
is
> what I have had all these years, and having found the symptoms of
> this I must agree.
>
> My sister is very over weight and I am very under weight, we do not
> live in the same part of the country, I live in England and my
> sister lives in Scotland.
>
> When she asked her GP how long she had this Dercums she was told it
> was diagnosed in 1995, and when she asked what is it her GP said I
> do not know, so she has been doing her own research on the web.
>
> I have too and I am trying to find a Doctor who would understand
> this disease, as i do not wish to go and tell my own GP I suspect
> this for fear of being told it is all in my head.
>
> So I am hoping someone on here can give me some advice, as to how
> best to approach this.
>
> My sister has had a number of lumps removed, where as I have not,
> and now thinking about our late mother, realize that she too had
> lumps removed, she was like me underweight, so the chances that
this
> is what she had too are high.
>
> Sorry this is so long winded, and look forward to hearing from you.
>
> Kind regards.
>
> Renee.

Hi Sharon,

This quote is actually taken from one of the articles I quoted - they
are both very long and have numerous other links - so it takes ages
to get through them.

I think this might be a link - perhaps even THE trigger. Many of us
are diagnosed with FMS, lupus, diabetes, RA, AS etc.

These bugs seem to imitate the immune system and therefore appear to
be capable of actually triggering the immune system response to
invasion by harmful bacteria and viruses. Perhaps we are triggering
this response to autoimmune diseases through these mycoplasmas or
perhaps the fact that we have these mycoplasmas has actually caused
all these different diseases in us. The experts have not decided
which came first - the chicken or the egg syndrome. Perhaps a
combination of the two.

Perhaps we have been weakened by these mycoplasmas over very long
periods of time and our bodily response is to form lipomas along
nerve pathways? Perhaps there is also a degree of demyelation which
has not been discovered in this Dercum's Disease which would make it
painful, but as they only ever investigate the lipoma or angiolipoma,
they never take out a nerve to examine and therefore never find that?

If I go back through my medical history, I can honestly say that I
have had mystery infections, mystery fungal infections etc., which
Doctors have had problems fighting and which have wreaked havoc in my
body. Nearly every organ has been under attack, at some time or
another. And, over months, they have slowly disappeared, only to have
a different infection start up elsewhere.

I am intrigued, but now we would need to get an Infectious Disease
Doctor interested in OUR disease in order to get answers. So little
is known about DD that I dare say few Doctors have ever even made the
connection. It just seems so logical, when so many of us have been
diagnosed with so many common factors. And I STILL believe that
Fibromyalgia is perhaps the beginning of DD, and that some go on to
develop it into full blown DD and others just stay at the FMS stage.
Anyway there seems to be so many common points between FMS, DD and
CFS that there has to be something in common. It could be that some
have stronger immune systems that can fight off the attack in FMS and
can stop it there. Indeed, there are loads of FMS patients who get
better over time - as with CFS. It just seems to be us that do not
get over our tumours, which eventually go on to multiply and cause us
such distress.

I am rambling - didn't sleep last night from brain overload!!!

Any ideas anyone?

Cynthia
--- In Dercums_Disease@yahoogroups.com, Shari <ShariCN@y...> wrote:
> Cyn,
>
> Very interesting...I'm just starting some reading and found this
from the following website (although I don't know how reputable the
website is I though the information was intriguing)
http://www.immunesupport.com/library/showarticle.cfm?ID=3066:
>
>
> Currently, other prominent researchers are corroborating the role
of mycoplasma in disease. The number of known conditions in which
mycoplasmas play a role is growing, thanks to advances in detection.
Mycoplasmas are now said to be contributors, or at least cofactors,
in a number of conditions, including CFS/CFIDS, fibromyalgia syndrome
(FMS), lupus, multiple sclerosis (MS), psoriasis, scleroderma,
Chrohn's diseases, solid cancers, leukemia, lymphoma, Amyotrophic
Lateral Sclerosis (ALS), pelvic inflammatory disease (PID), asthma,
atypical pneumonia, Sjogren's syndrome, interstitial cystitis,
Alzheimer's and cardiovascular diseases. Mycoplasmas have also been
associated with a variety if autoimmune diseases that can cause
definite changes in nerve conduction, demyelation (a degenerative
process that erodes away the myelin sheath that normally protects
nerve fibers) and sensitivity.
> Dr. Nicolson says that the role of mycoplasmas in various illnesses
and diseases is now gradually being accepted, especially in those
once long-suspected as "psychological." Acceptance is due to the
recognition that symptoms cannot be explained solely by psychological
criteria, and because discrete clinical markers have been discovered.
For example, the vascultitis (inflammation of blood vessels) found in
mycoplasma-positive patients correlates with evidence of mycoplasma-
induced abnormalities in blood cells and proteins related to blood
clotting.
> That sounds like quite a laundry list of diseases.  Who knows if DD
is among them?!  The part about degeneration of nerve sheaths could
explain some of the pain we have...
>
> Shari
>
> feisty_in_yorks <c_prentice2003@y...> wrote:
> Just following up on my thoughts........
>
> In another article which follows up on cellular malformations
etc....
> there was this interesting extract  :
>
> Other biological properties of mycoplasmas have been implicated as
> virulence determinants and include 1) generation of hydrogen
peroxide
> and superoxide radicals by adhering mycoplasmas, which induces
> oxidative stress, including host cell membrane damage; 2)
competition
> for and depletion of nutrients or biosynthetic precursors by
> mycoplasmas, which disrupts host cell maintenance and function; 3)
> existence of capsule-like material and electron-dense surface
layers
> or structures, which provides increased integrity to the mycoplasma
> surface and confers immunoregulatory activities; 4) high-frequency
> phase and antigenic variation, which results in surface diversity
and
> possible avoidance of protective host immune defenses; 5) secretion
> or introduction of mycoplasmal enzymes, such as phospholipases,
> ATPases, hemolysins, proteases, and nucleases into the host cell
> milieu, which leads to localized tissue disruption and
> disorganization and chromosomal aberrations; and 6) intracellular
> residence, which sequesters mycoplasmas, establishes latent or
> chronic states, and circumvents mycoplasmicidal immune mechanisms
and
> selective drug therapies (1,2,71,72).
>
> So it would seem that not only these mycoplasmas can actually live
> off and in cells, they then cause all sorts of disorders and
> disruptions of cellular activity.
>
> I was just wondering whether they are capable of enlarging lipid
> cells and multiplying them into lipomas and angiolipomas to make up
> our various bumps! As they have no definite shape they could
possibly
> multiply the fat cells in muscle cells thus causing pain long
before
> they could be discovered or even detected.
>
> Any ideas anyone ???
>
> Cynthia
>
>
>
>
> SPONSORED LINKS
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Hello everyone,

My name is Renee, and I have joined your group in hope I can find
help in UK.

I have been ill for a great number of years, and been classed as an
idiot by most doctors I have seen.

I was diagnosed with Fybromyalga, a long time ago,and recently my
sister was told she had Dercums Disease and she is convinced this is
what I have had all these years, and having found the symptoms of
this I must agree.

My sister is very over weight and I am very under weight, we do not
live in the same part of the country, I live in England and my
sister lives in Scotland.

When she asked her GP how long she had this Dercums she was told it
was diagnosed in 1995, and when she asked what is it her GP said I
do not know, so she has been doing her own research on the web.

I have too and I am trying to find a Doctor who would understand
this disease, as i do not wish to go and tell my own GP I suspect
this for fear of being told it is all in my head.

So I am hoping someone on here can give me some advice, as to how
best to approach this.

My sister has had a number of lumps removed, where as I have not,
and now thinking about our late mother, realize that she too had
lumps removed, she was like me underweight, so the chances that this
is what she had too are high.

Sorry this is so long winded, and look forward to hearing from you.

Kind regards.

Renee.

For Poe and anyone else interested:

Dr. Nico Mousdicas
IU Hospital Department of Dermatology
550 N. University Blvd., Suite 3240
Indianapolis IN  46202

317-274-7744

I don't think this is any relation to the Pimozide...

Curcumin is the yellow pigment of turmeric (Curcuma longa), the main
ingredient in curries. Curcumin is truly a "super antioxidant." In
some experimental studies it was up to 300 times more potent than
vitamin E. Curcumin is also an effective, yet safe, anti-inflammatory
agent. Curcumin is useful in any inflammatory condition and is also
recommended in cancer prevention and treatment adjunct (it can
prevent some of the side effects associated with certain chemotherapy
drugs), atherosclerosis, liver disorders, gallstones, and the
irritable bowel syndrome.

For medicinal effects, curcumin is recommended at a dose of 200 to
400 mg three times a day. Curcumin is available primarily in capsules
and tablets. Because the absorption of orally administered curcumin
may be limited, curcumin is often formulated in conjunction with an
equal amount of bromelain, which may possibly enhance absorption as
well as exert anti-inflammatory effects of its own. Combining
curcumin in an oil base such as lecithin, fish oils, or essential
fatty acids may also increase absorption.

Dear Feisty,

it certainly sounds logical, but right at this point in the day, I can
hardly put 2 logical thoughts together!  I went to the pool this
afternoon, and actually had to be helped up the ladder as I couldn't
muster enough strength to do it on my own.  Embarassing.  I have
printed out all the stuff, and will read it.  Thanks!

Judi

Currently, other prominent researchers are corroborating the role of mycoplasma in disease. The number of known conditions in which mycoplasmas play a role is growing, thanks to advances in detection. Mycoplasmas are now said to be contributors, or at least cofactors, in a number of conditions, including CFS/CFIDS, fibromyalgia syndrome (FMS), lupus, multiple sclerosis (MS), psoriasis, scleroderma, Chrohn’s diseases, solid cancers, leukemia, lymphoma, Amyotrophic Lateral Sclerosis (ALS), pelvic inflammatory disease (PID), asthma, atypical pneumonia, Sjogren’s syndrome, interstitial cystitis, Alzheimer’s and cardiovascular diseases. Mycoplasmas have also been associated with a variety if autoimmune diseases that can cause definite changes in nerve conduction, demyelation (a degenerative process that erodes away the myelin sheath that normally protects nerve fibers) and sensitivity.

Dr. Nicolson says that the role of mycoplasmas in various illnesses and diseases is now gradually being accepted, especially in those once long-suspected as “psychological.” Acceptance is due to the recognition that symptoms cannot be explained solely by psychological criteria, and because discrete clinical markers have been discovered. For example, the vascultitis (inflammation of blood vessels) found in mycoplasma-positive patients correlates with evidence of mycoplasma-induced abnormalities in blood cells and proteins related to blood clotting.

Just following up on my thoughts........

In another article which follows up on cellular malformations etc....
there was this interesting extract  :

Other biological properties of mycoplasmas have been implicated as
virulence determinants and include 1) generation of hydrogen peroxide
and superoxide radicals by adhering mycoplasmas, which induces
oxidative stress, including host cell membrane damage; 2) competition
for and depletion of nutrients or biosynthetic precursors by
mycoplasmas, which disrupts host cell maintenance and function; 3)
existence of capsule-like material and electron-dense surface layers
or structures, which provides increased integrity to the mycoplasma
surface and confers immunoregulatory activities; 4) high-frequency
phase and antigenic variation, which results in surface diversity and
possible avoidance of protective host immune defenses; 5) secretion
or introduction of mycoplasmal enzymes, such as phospholipases,
ATPases, hemolysins, proteases, and nucleases into the host cell
milieu, which leads to localized tissue disruption and
disorganization and chromosomal aberrations; and 6) intracellular
residence, which sequesters mycoplasmas, establishes latent or
chronic states, and circumvents mycoplasmicidal immune mechanisms and
selective drug therapies (1,2,71,72).

So it would seem that not only these mycoplasmas can actually live
off and in cells, they then cause all sorts of disorders and
disruptions of cellular activity.

I was just wondering whether they are capable of enlarging lipid
cells and multiplying them into lipomas and angiolipomas to make up
our various bumps! As they have no definite shape they could possibly
multiply the fat cells in muscle cells thus causing pain long before
they could be discovered or even detected.

Any ideas anyone ???

Cynthia

__________________________________________________
Do You Yahoo!?
Tired of spam? Yahoo! Mail has the best spam protection around
http://mail.yahoo.com

Just following up on my thoughts........

In another article which follows up on cellular malformations etc....
there was this interesting extract  :

Other biological properties of mycoplasmas have been implicated as
virulence determinants and include 1) generation of hydrogen peroxide
and superoxide radicals by adhering mycoplasmas, which induces
oxidative stress, including host cell membrane damage; 2) competition
for and depletion of nutrients or biosynthetic precursors by
mycoplasmas, which disrupts host cell maintenance and function; 3)
existence of capsule-like material and electron-dense surface layers
or structures, which provides increased integrity to the mycoplasma
surface and confers immunoregulatory activities; 4) high-frequency
phase and antigenic variation, which results in surface diversity and
possible avoidance of protective host immune defenses; 5) secretion
or introduction of mycoplasmal enzymes, such as phospholipases,
ATPases, hemolysins, proteases, and nucleases into the host cell
milieu, which leads to localized tissue disruption and
disorganization and chromosomal aberrations; and 6) intracellular
residence, which sequesters mycoplasmas, establishes latent or
chronic states, and circumvents mycoplasmicidal immune mechanisms and
selective drug therapies (1,2,71,72).

So it would seem that not only these mycoplasmas can actually live
off and in cells, they then cause all sorts of disorders and
disruptions of cellular activity.

I was just wondering whether they are capable of enlarging lipid
cells and multiplying them into lipomas and angiolipomas to make up
our various bumps! As they have no definite shape they could possibly
multiply the fat cells in muscle cells thus causing pain long before
they could be discovered or even detected.

Any ideas anyone ???

Cynthia

I have now tried to post this three times....

I have now been reading and analysing this text for two hours. It
explains just about my whole life story which Doctors have told me so
many times - its in your head - please please have a look and tell me
what you think.

Please could you all have a read and see what you think - Have I
found the connecting factor which has escaped even our Doctors??????

Please at least to attempt to read through these articles - they are
huge but I am sure it concerns us all!!!

http://www.rain-tree.com/myco.htm
http://www.rain-tree.com/fibromyalgia.htm

This is an extract which links fibromyalgia to this and why not DD to
FMS and this??
                           ----------------
The Correlation between Fibromyalgia and Mycoplasmas


Mycoplasmas require a large amount of cholesterol and other sterols
for growth and reproduction. If mycoplasmas are present and are
competing for these sterols intracellularly, less is available to the
body and especially the neuroendocrine system for the sythesis and
manufacture of steroids like estrogens, growth hormones and cortisols
which many FMS patients have been found to be deficent in.

Mycoplasmas also need and utilize proteins derived from amino acids.
Amino acids are the core building blocks in the neuroendocrine system
for the synthesis of most chemicals produced and used in the complex
intricate pathways of the neuroendocrine system including thyroid
hormone production and other chemicals taken up and used in the HPA.
This may cause the deregulation of the neuroendocrine system thru the
loss of vital nutrients required to maintain regulation.

Mycoplasma maintains a defense mechanism which encodes tryptophan to
hide from normal immune responses. If enough tryptophan was utilized
from host cells in the neuroendocrine system for this purpose, less
would be available to the body for the normal synthesis of tryptophan
to seratonin, thus possibly deregulating or lowering seratonin levels
and causing depression and sleep disorders most FMS patients present.

Mycoplasmas have the ability to attached to any cell in the body and
cause that cell to malfunction, acting differently, thereby causing
different interactions with other cells. If mycoplasmas invaded and
attached to various cells in endocrine organs, it could cause the
widespread deregulation of the entire endocrine system described in
the previous research shown above, because of the complex
interactions between these organs and the chemicals they produce and
utilize.
                    ------------------------------

There is loads more to read and analyse and I fully intend to do so
when I have not been active all day and my brain is not in DD fog...
If only you were all local and we could just sit and chat!

I HONESTLY BELIEVE THIS IS THE BIG MISSING LINK - Have I gone mad?

Looking forward to your comments!

Cynthia

And could it perhaps be what this drug Judi's doc wants to put her on?

Judi,

I am kind of between doctors right now as my decent doc at Grady has
graduated and moved on. It might help with my transition
and 'training' of a new doc if I could get him or her in contact
with your Dr. M. Would he mind, do you think? And then maybe my new
doc would be willing to try the drug on me in the future if it works
for you.... Because you are right, it needs to be tried to find out
if it will work. All of us stand to benefit.

Let me know....

Poe (Judith)

--- In Dercums_Disease@yahoogroups.com, "nonny46" <nonny46@y...>
wrote:
> Dear Dorrit,
>
> I really do appreciate your concern!  It means a lot to me that
someone
> I have only met on a computer screen cares enough about me to
express
> that concern.  Believe me, I am taking my time before agreeing to
the
> treatment--will talk to our new family doc next week, and have the
> cardiologist evaluation.  I don't have to let Dr. Mousdicas know
until
> August 26.  But SOMEONE has to try these things, and in order to
get a
> good idea of what the effects are, more than one person needs to
be
> willing.  IF I decide to go ahead with it, I will keep you all
informed
> of any results, positive or negative.
>
> Today is a beautiful, clear, mild day, and I'm going to enjoy it!
>
> Peace,
> Judi

Dear Dorrit,

I really do appreciate your concern!  It means a lot to me that someone
I have only met on a computer screen cares enough about me to express
that concern.  Believe me, I am taking my time before agreeing to the
treatment--will talk to our new family doc next week, and have the
cardiologist evaluation.  I don't have to let Dr. Mousdicas know until
August 26.  But SOMEONE has to try these things, and in order to get a
good idea of what the effects are, more than one person needs to be
willing.  IF I decide to go ahead with it, I will keep you all informed
of any results, positive or negative.

Today is a beautiful, clear, mild day, and I'm going to enjoy it!

Peace,
Judi

I posted my experience using the generic(?)name Orap some time ago.
It was dismissed pretty unanimosly by this group after members read
its potential side effects.  Thought it should resurface again since
Judi's MD suggested its use.
--- In Dercums_Disease@yahoogroups.com, "Dorrit Hvam" <fiori68@y...>
wrote:
> Hi
> I just find it odd that you have found something that helps you so
> much and never told about it? (To my memory)
> But considering that it did not help the other patient, it does
not
> seem to be THE solution that we are hoping for.
>
> Judy, the guinea pig: Please be careful. You are exposing your
body
> to a lot of medicines these days. Not that I want to discourage
you,
> but you must not weaken youir body too much by being our guinea
> pig....
> says a very tired Dorrit whose fatigue was brought on by something
> so ridiculous as having a new kitchen floor coverage, and I did
not
> do anything. Just like a flat tyre tonight.
>
>
> --- In Dercums_Disease@yahoogroups.com, "ejankowitz" <ejanko@a...>
> wrote:
> > I seldom post but wanted to comment and share my personal
> experience
> > with Pimozide AKA Orap.  Have been taking it for DD as
recommended
> by
> > a derm who evauated me at a conference at University of PA close
> to 2
> > years ago.  Dr. Keblonzer has since become my derm who I see
> > regularly.  I have had great success with Pimozide; very
effective
> > with neurologic pain, general decrease in overall pain and no
new
> > growth.  I am able to continue to work full time and lead a full
> and
> > semi-active life.  Side effects of the drug seem scary, but I
have
> > experienced none of those listed and am reassured by my MD that
> these
> > do not occur at the low dosages that we are given.  It has made
a
> > great difference in my life and I would recommend you trying it
to
> > see if it helps.  BTW: Dr. Keblonzer treated another DD patient
> with
> > Pimozide with unsuccessful results.  I guess we're all different.
> > --- In
> > Dercums_Disease@yahoogroups.com, "nonny46" <nonny46@y...> wrote:
> > > Hi group,
> > >
> > > I saw Dr. Mousdicas today, and he wants me to try a
medication.
> It
> > > was kind of funny, because I had told him about how badly many
> of
> > us
> > > have been treated by doctors, that the doctors as much as tell
> us
> > we
> > > are nut cases, and then he laughs and tells me that he has a
new
> > > medication he wants me to try....and it is an anti-psychotic!!
> > >
> > > Seriously, it is called Pimozide, and has recently been found
> > > effective in reducing MELANOMAS, which are extremely dangerous
> > > buggers.  It has also been found effective in treating
> trigeminal
> > > neuralgia and post herpetic neuralgia.  I have to have an ECG
> > > adminstered by a cardiologist (and he insists on personally
> > speaking
> > > with the cardiologist) as the drug can cause trouble if a
person
> is
> > > prone to arrythmia.  So, after I have read up on the drug, had
> my
> > > ECG, and Ron and I have had a chance to discuss it with our
new
> > > family doc, and after I find out if I need surgery on my
> shoulder,
> > > then IF I decide to go ahead, it will be a chance to see if it
> > helps
> > > with the DD.  At the very least, it may be more effective
> against
> > the
> > > pain.  I would start at the smallest dosage, and increase to a
> > > somewhat larger dose, but nowhere near the highest dosage.
> > >
> > > I am so grateful to have found a doctor who believes in
helping
> me,
> > > and he reiterated that he DOES believe this is a very real,
and
> > very
> > > dangerous disease, and he has no intention of giving up on me.
> > >
> > > Hey, at the very least, maybe I won't be psychotic?
> > >
> > > Time to go rest--I drove 120 miles by myself today and then
came
> > home
> > > to take care of the triplets for 3 hours.
> > >
> > > Judi