Microbes and Mental Illness
By Robert C. Bransfield, M.D.
Microbes
are the greatest predator of man. As medical technology improves, there is
increasing recognition that infectious disease contributes not only to acute,
but also chronic relapsing illness and mental illness. The evidence to support
this is a combination of insights from theoretical biology (particularly
Darwinian medicine), research, and direct clinical observations.
We
lead our entire lives surrounded by microbes. In a state of health, there is a
balance, a reasonable resistance to infectious disease, and a peaceful
co-existence. In contrast, with
infectious disease, there is an imbalance between the
threat posed by microbes and host defenses. This balance is affected by
environmental factors (including exposure to pathogens) and a number of host
factors such as genetics and/or increased vulnerability as a result of a state
of chronic stress. Although the stress response is adaptive in a short time
frame to allocate resources during a crisis, if the stress response is
persistent, rather than cyclic, it further increases vulnerability to disease.
The
most common sequence of disease begins with a vulnerability and an exposure to
one or more stressors. The vulnerability may commonly include genetic and/or
increased vulnerability as a result of chronic stress. As a result of these and
other vulnerabilities, the microbe more easily penetrates the host's defenses
and an initial infection may then occur.
Although
infection may occur from microbes that are always present in the environment, a
greater number of organisms or more virulent organisms further increase risk.
Acute infections are most noteworthy in general medicine. However, the course
of the infection most relevant to psychiatry includes injury from a prior
infection; chronic, low-grade, persistent relapsing infections; or the
persistence of the infectious agent in
the inactive state. When persistent, relapsing infection occurs, there may be
extended period of latency followed by some triggering event(s) (i.e.: chronic
stress, injury, surgery, or other infectious agents), which may then cause the
activation of the infectious agent(s)
and the progression of the pathological process.
Some
injury in infectious disease is a result of toxic products or direct cell
injury, but a significant amount of injury is a result of host defenses gone
awry in response to the infection. Neural injury may occur by a variety of
mechanisms, which include vasculitis, direct cell injury, toxins, inflammation,
cytokines, autoimmune mechanisms, incorporation of parasite DNA into host DNA,
and excitotoxicity. This injury leads to a vicious cycle of disease, resulting
in dysfunction of associative and/or modulating centers of the brain. Injury to
associative centers more commonly causes cognitive symptoms, while injury to
modulating centers more commonly causes emotional and allocation of attention
disorders.
Psychiatric
syndromes caused by infectious disease most commonly include depression, OCD,
panic disorder, social phobias, variants of ADD, episodic impulsive hostility,
bipolar disorders, eating disorders, dementia, various cognitive impairments,
psychosis, and a few cases of dissociative episodes.
In
clinical experience, the link between infectious disease and psychopathology
has been
an issue with Lyme disease, syphilis, babesiosis,
ehrlichiosis, mycoplasma pneumonia, toxoplasmosis; stealth virus, borna virus,
AIDS, CMV; herpes, strep and other unknown infectious agents. In the collective
database of patients demonstrating psychiatric symptoms in response to
infectious disease, the majority of the cases has been infected by ticks.
Aristotle referred to ticks as "filthy disgusting animals" (1). They
spend their lives living in dirt, feeding on the blood of mice, rats, and other
wild animals (2). When they bite humans, they pose a risk of injecting an
infectious cocktail of pathogens into the host.
Patients
with psychiatric symptoms from tick-borne diseases are most commonly infected
by Borrelia burgdorferi, (Bb) the causative agent of Lyme disease and quite
often other coinfections-infections. There is an increasing recognition that
many chronic relapsing infections are complex interactive infections in which
microbes interact with each other in a manner that contributes to the disease
process. The models most commonly discussed are coinfections associated with HIV and tick-borne
coinfections. For example, coinfections associated with Lyme disease may be
acquired at the same time, before or after the Bb infection. Interactive
infections, however, is a more accurate term than coinfections, since these
infections invariably cause an interaction that changes the disease process.
To
understand coinfections, we need to begin by defining each disease separately.
This,
of course, is an area of much controversy in regard to
late stage chronic relapsing Lyme disease. A similar controversy exists in
regard to other chronic infections. It is difficult to explain how interaction
occurs when there is such disagreement defining the clinical syndrome and
pathophysiology associated with each infection separately.
A
couple of years ago, other tick-borne diseases were not considered to be very
significant in contributing to chronic, relapsing Lyme disease. Once there was
a greater focus upon these organisms, it became clear that coinfections were a
significant issue. We can better understand chronic, relapsing diseases such as
Lyme disease by taking a closer look at interactive coinfections, host
vulnerability, and host response that contributes to the disease process.
Some
very interesting work is being
In
summary, the complexities of these issues teach us humility. To better
understand the
clinical syndrome associated with these infections,
internists need to recognize the significance of mental symptoms in chronic
interactive infections and psychiatrists need to better appreciate the role of
microbes in causing mental illness.
(1)
Adapted from Burrascano, J., The New Lyme Disease Diagnostic Hints and
Treatment Guidelines for Tick-Borne Illness, l2th Edition, copyright 10/98.
(2)
Burgdorfer, W.B., Increased Evidence of Mosquito/Spirochete Associations; 11th
International Scientific Conference on Lyme Disease and other Spirochetal &
Tick-Borne Disorders.
(3)
Discussion with Dr. John Martin
(4) Discussion with Dr. Linda Mattman