Download Autoimmune Disease Infections and Women

Communicable Disease News
Editor: Dorothy MacEachern, MS, MPH
1101 W. College Avenue, Room 360
Spokane, WA 99201-2095
509-324-1442
[email protected]
Lord, make me an instrument of your peace.
Where there is hatred let me sow love;
where there is injury, pardon;
where there is doubt, faith;
where there is despair, hope;
where there is darkness, light;
and where there is sadness, joy.
--St. Francis of Assisi
November 200
4
2004
Autoimmune Disease Infections and Women
Autoimmune diseases are the third most common
category of disease in the United States after cancer and
heart disease; they affect approximately 5–8% of the
population or 14–22 million persons. Autoimmune
diseases can affect virtually every site in the body,
including the endocrine system, connective tissue,
gastrointestinal tract, heart, skin, and kidneys. At least
15 diseases are known to be the direct result of an
autoimmune response. In several instances, such as
rheumatoid arthritis, multiple sclerosis, and myocarditis,
the autoimmune disease can be induced experimentally
by administering self-antigen in the presence of adjuvant
(collagen, myelin basic protein, and cardiac myosin,
respectively) .
Autoimmune diseases tend to cluster in families and
in individuals (a person with one autoimmune disease is
more likely to get another), which indicates that common
mechanisms are involved in disease susceptibility.
Genetic background appears to account for about one
third of the risk of autoimmune disease. This estimate is
based on studies that compared genetically identical,
monozygotic twins to nonidentical, dizygotic pairs, for
which the concurrence rate can be as low as 2% to 7%.
Noninherited factors may account for the remaining
(approximately 70%) risk of developing an autoimmune
disorder.
Soon after autoimmune diseases were first recognized
more than a century ago, researchers began to associate
them with viral and bacterial infections. A body of
circumstantial evidence links diabetes, multiple sclerosis,
myocarditis, and many other autoimmune diseases with
preceding infections; many different microorganisms
have been associated with a single autoimmune disease,
which indicates that more than one infectious agent can
induce the same disease through similar mechanisms (See
table below). Since infections generally occur well before
the onset of symptoms of autoimmune disease, clinically
linking a specific causative agent to a particular
autoimmune disease is difficult. This raises the question
of whether autoimmune diseases really can be attributed
to infections.
To address this question, autoimmunity first needs to
be defined. Autoimmune disease occurs when a response
against a self-antigen(s) involving T cells, B cells, or
autoantibodies induces injury either systemically or
against a particular organ. Understanding of autoimmune
diseases is hindered by the fact that some level of
autoimmunity, in the form of naturally occurring
autoantibodies and self-reactive T and B cells, is present
in all normal persons. Thus, on a proportional basis,
developing autoimmune disease is the relatively
uncommon consequence of a common autoimmune
response. Although an autoimmune response occurs in
most persons, clinically relevant autoimmune disease
develops only in some persons.
So, how can infections induce autoimmune disease?
A mechanism often called on to explain the association
of infection with autoimmune disease is “molecular
mimicry,” that is, antigens or epitopes of the
microorganism closely resemble self-antigens. The
induction of an immune response to the microbial antigen
thus results in cross-reaction with self-antigens and
induction of autoimmunity. Although epitope-specific
cross-reactivity between microbes and self-tissues has
been shown in some animal models, molecular mimicry
has not been clearly demonstrated to occur in human
diseases. Another possibility is that microorganisms
expose self-antigens to the immune system by directly
damaging tissues during an active infection. This
mechanism has been referred to as the “bystander effect”.
However, whether pathogens mimic self-antigens, release
sequestered self-antigens, or both, is difficult to
determine.
In addition to antigen-specific mechanisms,
nonspecific mechanisms could also lead to autoimmunity
after infection. To determine whether infection can lead
to autoimmune disease, direct evidence (e.g., the ability
to transfer autoimmune disease), indirect evidence (e.g.,
the ability to reproduce autoimmune disease in animal
models), and circumstantial evidence (e.g., the association
of autoantibodies with disease in appropriate clinical
settings) should be considered. The best evidence so far
that infections can induce autoimmune diseases comes
from animal models. In most animal models of
autoimmunity, including myocarditis, disease has been
transferred to naïve animals with autoimmune cells
(splenocytes or T cells), autoantibodies, or both, which
provides compelling evidence that infections induce
autoimmune diseases by immune-mediated mechanisms.
It has been known for some time that the basic
immune response differs between men and women, with
women producing a more vigorous immune response and
increased antibody production. Women are more
susceptible to autoimmune diseases, but autoimmune
diseases that develop in men often are more severe. Many
animal models of autoimmune disease have shown a
similar sex bias.
Sex hormones, such as estrogen, testosterone, and
progesterone, may mediate most of the sex-biased
differences in the immune response. The precise
interaction between hormones and the innate immune
response after infection is poorly understood. However,
in-vitro studies of immune cells cultured in the presence
of hormones have shown that estrogen significantly
increases proinflammatory cytokine production. Thus, the
elevated immune response in women may even further
Infe ctions in Humans As s ociate d with Autoimmune Dis e as e s
Dis e as e
Infe ction
Multiple sclerosis
Epstein- Barr virus (EBV), measles virus
Lyme arthritis
Borrelia burgdorf eri
Type I diabetes
Coxsackie virus B4, rubella virus, cytomegalovirus (CMV), mumps virus
Rheumatoid arthritis
Escherichia coli, mycobacteria, EBV, hepatitis C virus (HCV)
Lupus erythematosis
EBV
Myocarditis
CB3, CMV, chlamydia
Rheumatic fever/myocarditis
Streptococci
Chagas' disease/myocarditis
Trypanosoma cruzi
Myasthenia gravis
Herpes simplex virus, HCV
Guillain- Barré syndrome
CMV, EBV, Campylobacter spp.
amplify the adjuvant effect of infection,
thereby increasing the possibility that
chronic autoimmune disease will
subsequently develop in women. With
the increase in the number of
autoimmune cases diagnosed in recent
years, the possible role of infections in
exacerbating disease, particularly in
women, is of rising concern.
Excerpted from Fairweather D, Rose
NR. Women and autoimmune diseases.
Emerging Infectious Diseases, 2004
November. Available from http://
www.cdc.gov/ncidod/EID/vol10no11/040367.htm
TRAINING AND EDUCATION UPDATES-Satellite Downlinks:
Noon-2:00 pm, “Meth Madness: What Every Healthcare Worker Should Know,” SRHD Room 360.
Nov 17:
Nov 18:
10-Noon, “Rapid Testing: Advances for HIV Prevention,” SRHD Room 360.
Dec 7:
11:00 am-1:30 pm, “Crisis & Emergency Risk Communication, Part I” SRHD Room 360.
Dec 14:
11:00 am-1:30 pm, “Crisis & Emergency Risk Communication, Part II” SRHD Room 360.
Welcome! Jennifer Polello, our new Regional Learning & Support Specialist, joined us on November 1. Jennifer comes to us
from SRHD’s Health Promotions Division, where she was the Tobacco Control and Prevention health educator. Visit
www.srhd.org/Region9Calendar to find broadcasts that are available on VHS or DVD. For more information call Jennifer
Polello at 324-1529, or email [email protected].
AIDS Case Reporting Changes
All states and areas have been reporting AIDS cases since 1986 or earlier. For surveillance purposes, AIDS cases
have always been counted as belonging to the geographic area where they were diagnosed with AIDS (which may not
reflect where they currently reside and receive services). If, for example, someone was first diagnosed with AIDS in
Washington and then moved to Oregon, they would still be counted as a Washington case. If the person moved to
Oregon and did not tell their health care provider they had been previously diagnosed in Washington, the case would
be counted in both states, resulting in duplication and contributing to artificial inflation of case numbers at the
national level.
To counter the problem, the Centers for Disease Control and Prevention (CDC) initiated the Interstate Deduplication
Project (IDEP) in 2002. CDC identified potential duplicates in the national database. Since they do not receive
names of those with AIDS, CDC sent the information to the states, who worked together to identify which cases were
duplicates. In total, 1,063 Washington State AIDS cases were determined to be the same person as at least one other
state’s case. As a result of completion of this exercise, 658 Washington State cases were retained with a local AIDS
diagnosis residence and 405 cases were assigned an Out of State diagnosis residence.
CASES OF SELECTED DISEASE REPORTED TO SPOKANE REGIONAL HEALTH DISTRICT, OCT 2004
THIS MONTH
LAST MONTH
THIS YEAR TO DATE LAST YEAR TO DATE
DISEASE
(Oct. 2004)
(Sept. 2004)
(Oct. 2004)
(Oct. 2003)
**0
**1
10
22
AIDS *cumulative--448 since Jan 1984
0
0
2
0
Borreliosis (Relapsing Fever)
0
4
48
65
Campylobacteriosis
86
84
944
825
Chlamydial STD
1
1
2
8
Enterohemorrhagic E. Coli
6
6
41
33
Giardiasis
14
13
133
87
Gonorrhea
0
0
3
6
Hepatitis A-acute
1
0
9
15
Hepatitis B-acute
0
2
18
39
Hepatitis B-chronic
28
22
300
374
Hepatitis C -acute and chronic
**0
**0
8
11
HIV *cumulative--136 since Dec 2001
0
0
0
2
Influenza (Sept 1--Aug 31)
0
0
0
0
Measles (Rubeola, Red)
0
0
5
3
Meningococcal Disease
0
0
0
0
Mumps
2
10
34
4
Pertussis (Whooping Cough)
0
0
0
0
Rubella (German Measles)
1
3
24
26
Salmonellosis
1
0
3
9
Shigellosis
1
0
3
3
Syphilis
**0
**0
3
4
Tuberculosis** (as of Sept 2004)
**Counts may be one month or more delayed
*HIV/AIDS cumulative totals adjusted to eliminate interstate duplicates, 10/2004
Clinic 324-1600
Communicable Disease 24-hour Confidential Report Line: 324-1449
HIV/AIDS Program 324-1542 TB Program 324-1614 Epidemiology 324-1442